Available PhDs

Finding BiomARKers of Canine Kidney Senescence (BARK)

Applications received up to Friday 6th March 2026, 12noon

Supervisor(s): Dr Katie Mylonas (The University of Edinburgh), Dr David Baird (The University of Edinburgh), Prof Jeremy Hughes (The University of Edinburgh), Dr Dylan Clements (The University of Edinburgh, Dr Geoff Culshaw (The University of Edinburgh)About the Project

Autophagy, Danger Signalling and Immune Dysregulation in Systemic Lupus Erythematosus (SLE)

Applications received up to Friday 27th February 2026, 12noon

Supervisor(s): Prof Mohini Gray (The University of Edinburgh)

Fully funded PhD Studentship at the Institute for Regeneration and Repair

A fully-funded PhD studentship to study at the Institute for Regeneration and Repair (IRR), a research institute based at the University of Edinburgh. Scientists and clinicians at IRR study tissue regeneration and repair to advance human health and reproductive outcomes. The Institute incorporates three leading research centres with a focus on regenerative medicine, inflammation, and reproductive health.

About the Project

Summary

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterised by chronic inflammation, type I interferon activation, and multi-organ involvement. Despite major advances in immunology, the cellular mechanisms that link immune cell stress to sustained inflammatory signalling in lupus remain incompletely understood.

This PhD project will focus on the role of defective autophagy in immune cells and how this contributes to aberrant danger signalling and interferon responses in SLE. Recent work from our group has shown that lymphocytes from patients with lupus exhibit impaired autophagy and mitochondrial stress, and that viable, stressed cells can activate STING-dependent interferon signalling in bystander cells via contact-dependent mechanisms. Understanding how these processes operate in human disease is critical for identifying new therapeutic targets and biomarkers.

The project has a clear translational aim: to improve understanding of immune dysregulation in lupus in ways that may ultimately inform better treatments for patients.

Project outline

A central unanswered question in lupus is why immune responses become chronically activated in the absence of overt infection. Emerging evidence suggests that immune cell stress, rather than antigen recognition alone, plays a key role in driving pathological inflammation.

This PhD project is based on the hypothesis that defective autophagy in lupus lymphocytes leads to abnormal cellular stress and danger signalling, which in turn activates innate immune pathways and sustains type I interferon responses. The student will work primarily with human immune cells from patients with SLE and healthy controls to investigate how impaired autophagy, mitochondrial dysfunction, and altered cell–cell interactions contribute to inflammatory signalling.

The work will combine cellular, molecular, and functional immunology approaches to define how stressed but viable immune cells activate bystander cells through cGAS–STING-dependent pathways. Where appropriate, the project will also explore whether pharmacological or metabolic interventions can normalise these responses. The overall aim is to generate mechanistic insights into lupus pathogenesis, maintaining a strong focus on human disease relevance.

Aims

Aim 1: Define autophagy defects and cellular stress in immune cells from patients with SLE
The student will characterise autophagy pathways, autophagic flux, and mitochondrial health in lymphocyte subsets from lupus patients and healthy controls using established cellular and biochemical assays.

Aim 2: Determine how stressed but viable lymphocytes activate innate immune signalling in bystander cells
This aim will investigate contact-dependent activation of cGAS–STING and type I interferon pathways in co-culture systems, focusing on danger signals released by autophagy-deficient cells.

Aim 3: Test whether modulation of autophagy or danger signalling can normalise inflammatory responses
The student will explore pharmacological or metabolic interventions targeting autophagy or STING signalling to assess their effects on immune activation and interferon production.

Training Outcomes

The student will receive comprehensive training in human immunology and translational research, including:

• Isolation and culture of primary human immune cells
• Flow cytometry and immune phenotyping
• Functional assays of autophagy, mitochondrial stress, and interferon signalling
• Co-culture and perturbation experiments
• Data analysis and interpretation in a clinically relevant context

The project is designed to provide strong training for a career in immunology or translational biomedical research.

References (selected background)

1. Hopfner KP et al. Molecular mechanisms and cellular functions of cGAS–STING signalling. Nat Rev Mol Cell Biol, 2020. https://doi.org/10.1038/s41580-020-0244-x
2. Rönnblom L, Leonard D. The interferon pathway in SLE: one key to unlocking the mystery of the disease. Lupus Sci Med, 2019;6:e000270. https://doi.org/10.1136/lupus-2018-000270
3. Tsokos GC et al. New insights into the immunopathogenesis of systemic lupus erythematosus. Nat Rev Rheumatol, 2016;12:716–730. https://doi.org/10.1038/nrrheum.2016.186

Contact details

For more information, please contact: Professor Mohini Gray at Mohini.Gray@ed.ac.uk
Institute for Regeneration and Repair, The University of Edinburgh

Funding Notes

The successful candidate will receive a fully-funded PhD studentship supported by the Lorna May Smith Charitable Trust.

The studentship provides funding for up to four years, covering UK Home tuition fees, a stipend at a rate commensurate with UKRI, and research and travel costs.

This studentship is available to candidates eligible for UK Home fee status.

Recruitment

This project will be suited to students with a strong interest in immunology, autoimmune disease, and translational biomedical research. Applicants should be of outstanding academic merit and research potential.

Applicants should have obtained, or expect to obtain, a first-class or upper second-class UK honours degree (or equivalent non-UK qualification) in a relevant subject area such as biomedical sciences, immunology, biology, or a related discipline.

Previous research experience in areas such as cell culture, flow cytometry, molecular biology, or human immunology is desirable but not essential. Enthusiasm for working with primary human samples and an interest in mechanisms of immune dysregulation in disease are particularly encouraged.

How to apply

• Please send your CV and personal statement before 27 February 2026 (12 noon, UK time) by email to: IRRSchoolPGR@ed.ac.uk. Please include “PhD Studentship – Lupus IRR” in the subject line.
• You are required to ask two relevant referees to send a reference letter to the same email address, using ‘Reference for PhD Studentship – Lupus IRR” in the subject line. The letter should be dated and on letterhead paper.

We regret that we are unable to respond to unsuccessful or incomplete applications.

Interviews

Interviews are expected to take place in the week of 30th March 2026.

Application deadline: 27 February 2026, 12noon (UK time).

Uncovering how regulation of endogenous retroelements shapes bat immune responses

Closed for applications 

Supervisors: Dr Richard Sloan (The University of Edinburgh), Dr Matt Brook (The University of Edinburgh), Dr Wanlu Liu (ZJE Joint Institute), ZJE

Project location

Hugh Robson Building, George Square.

Project description

The aim of this project is to understand how genomic endogenous retroelements influence bats’ unique immune responses and thus their role as viral reservoirs. Bats have been the source of viral spillovers such as SARS-CoV-2, Marburg virus, and Nipah virus. Their ability to cope with the metabolic stress of powered flight is thought to necessitate an anti-inflammatory immune state.

Endogenous retroelements propagate themselves throughout genomes, causing genetic disruption and inflammatory responses to their nucleic acids. These inflammatory responses can shape innate and adaptive immunity, impacting areas like lymphocyte development, senescence, and B/T cell function. Generally, endogenous retroelements are then suppressed by host epigenetic and post-transcriptional mechanisms.

Our analysis of mammalian genomes shows that genes coding for proteins that regulate retroelement expression (e.g. HUSH complex) are under positive selection, suggesting the evolution of altered function in bats. Potentially, the strong selection pressure to curtail inflammation in bats leads to selection for endogenous retroelement-regulatory gene products to be more suppressive. Our preliminary data also shows altered transposon integration patterns in some bat species.

We will conduct evolutionary genetic analysis with newly sequenced bat genomes to further identify bat retroelement regulators with altered functions. Using RNA sequencing and molecular biology methods, we will then examine effects on epigenetic marks, retroelement transcription, and RNA metabolism. Next, we will explore how variations in retroelement expression affects antiviral and inflammatory responses in bat cell lines and iPSC-derived immune cells.

Overall, this research will reveal how differential regulation of endogenous retroelements underpins bats’ status as key viral reservoirs.

Approaches used in project

This project will use a mix of computational, molecular, and immunological approaches. Genes of interest will be identified through positive selection analysis of mammalian genomes. Panels of cloned endogenous retroelement regulators will be screened for effects on human and bat endogenous retroelements. Both qPCR and RNA sequencing will be used to determine levels of endogenous retroelement RNA in knockout bat cell lines. Alternative qPCR or sequencing technologies to define changes in transcription or epigenetic modifications may also be used. Innate immune responses will be measured in cell lines as well as bat iPSC derived immune cells.

Relevant references for project background

1. Bat genomes illuminate adaptations to viral tolerance and disease resistance Morales A et al. Nature. (2025) 638, 449–458
2. Lessons from the host defences of bats, a unique viral reservoir. Trent-Irving A et al. Nature. (2021). 589, 363–370
3. Alternative splicing expands the antiviral IFITM repertoire in Chinese horseshoe bats. Mak N, Zhang D, Li C, Rahman K, Datta SAK, Taylor J, Liu J, Shi Z, Temperton N, Trent-Irving A*, Compton AA*, Sloan RD*. PLoS Pathogens. (2024) 20,12: e1012763.
4. MORC1 represses transposable elements in the mouse male germline. Pastor WA, Stroud H, Nee K, Liu W, Pezic D, Manakov S, Lee SA, Moissiard G, Zamudio N, Bourc’his D, Aravin AA, Clark AT, Jacobsen SE. Nature Communications. (2014). 5:5795.
5. Neutrophil-derived alpha defensins control inflammation by inhibiting macrophage mRNA translation. Brook M, Tomlinson GH, Miles K, Smith RWP, Rossi AG, Hiemstra PS, van 't Wout EFA, Dean JLE, Gray NK, Lu W, Gray M. Proceedings of the National Academy of Sciences. (2016). 113(16):4350-4355.

How to apply

Based in the Edinburgh Medical School, University of Edinburgh you will have the opportunity to work with leading research groups while also developing your skills in transnational education. The studentships are fully funded for 4 Years including full fees (home or overseas), UKRI-level stipend and generous research costs.

Alongside their PhD project, students will be supported in the development of their skills in TNE towards AFHEA accreditation. This will include short (typically 2 visits totalling 4-6 weeks per year) research and educational visits to our ZJE Joint Institute in China supported by their PhD supervisory team.

Applicants are required to discuss projects with prospective supervisors before submitting their application.

Candidates must meet University of Edinburgh PhD requirements including English language proficiency and acceptance is conditional on award of 2:1 degree classification (or similar) in a Biomedical related undergraduate Honours degree programme.

To apply, email a single PDF document to ZJEPGSupport@ed.ac.uk by 12 noon on Friday 30th January 2026 that includes:

1. your CV
2. a 1 page statement of why you wish to pursue a PhD, including a ranking of up to 3 projects you are interested in following your discussion with prospective supervisor(s)
3. a 1 page statement of how developing your transnational educational skills as part of your PhD will support your longer term career aspirations. 

You can view all projects associated with this programme here.

Shortlisted candidates will have further opportunity to meet with prospective PhD supervisors of their ranked projects at interview.

Clinically actionable insights into endometriosis symptom trajectories using longitudinal self-reports, biological samples, and data from digital technologies

Closed for Applications  

Supervisor(s): Prof Thanasis Tsanas, Prof Andrew Horne & Prof Philippa Saunders

Centre/Institute: Usher Institute

Background

Endometriosis is a chronic condition associated with debilitating pain, fatigue, and heterogeneous symptom manifestation. It affects ~10% women of reproductive age, may take ~8 years to diagnose, and symptom progression typically relies on sparse clinical assessments. There is an urgent call for action to capitalize on recent biological and technical developments to improve diagnosis and symptom monitoring [1]. We have recently proposed developing a pioneering framework to transform endometriosis assessment capitalizing on digital technologies [2]. Standardised patient reported outcome measures (PROMs) where people living with endometriosis regularly self-report on their symptoms are increasingly used to monitor symptom severity progression. Over time, these can provide useful insights into patients’ own self perception of pain and diverse symptoms. Similarly, regularly collected biological samples may offer insights into symptom trajectories over time. The proliferation of new digital health technologies, including wearable sensors, has been gaining increasing momentum [2]. The use of digital health technologies can provide additional continuous and passively collected data, which can be mined to obtain new insights complementing clinical reports, lab tests, and PROMs. We recently reported on the largest study of-its-kind endometriosis study, demonstrating how self-reports and wearable sensors can provide longitudinal insights into symptom trajectories and objective surgical intervention assessments [3]. Specifically, we have developed new signal processing and statistical machine learning algorithms towards assessing physical activity, sleep, and diurnal rhythm variability to process actigraphy data, and demonstrated how the extracted characteristics could complement and inform clinical assessments. Additionally, we have been developing information fusion and deep learning algorithms to mine multimodal data in other research applications [4], which could be deployed in the endometriosis project too. Building on projects that the supervisory team is involved (e.g. the £4m ADVANTAGE project and the £6m EUmetriosis project) this is an exciting time as we have collected (with further data collection ongoing) the largest longitudinal multimodal datasets in endometriosis.

Aims

The recruited student will further extend the algorithmic framework developed in the group to mine multimodal data (PROMs, lab-based results and clinical reports, data from wearables), to provide new clinically useful insights into endometriosis towards facilitating (a) longitudinal symptom monitoring, (b) objective intervention assessments, and (c) cohort stratification. The student will explore different datasets: (i) multimodal data from the ENDO1000, EUmetriosis and ADVANTAGE projects that the supervisory team are leading (collectively >500 people living with endometriosis), (ii) additional unique actigraphy datasets to facilitate algorithm development with external measures of ground truth (e.g. in terms of actigraphy and polysomnography data, >100 participants already collected). We envisage the large multimodal longitudinal datasets will enable patient stratification towards facilitating a more personalized treatment (precision medicine). The outputs of the analysis will be disseminated through our PPIE network (led by project supervisors Horne and Saunders), inform broader ongoing studies such as the EUmetriosis project, and potentially directly translated/embedded into NHS practice. The project is particularly suitable to students with interests in (multimodal) signal processing, time-series analysis and machine learning. At the end of this PhD project, the student will have a unique and transferable skillset in signal processing, mining multimodal data, and developing statistical machine learning methods, which is highly desirable in both academia and industry.

Training outcomes

• Practical understanding of the problems at the interface of clinical practice and data analytics, including the language barrier with niche terminology on both ends
• Developing expertise in actigraphy, time-series analysis, signal processing, information fusion, and statistical machine learning to tackle large-scale challenging problems
• Programming skills: transforming algorithmic concepts to software tools, and developing interfaces which can be used by experts and non-experts to facilitate data analysis

References

1. P.T.K. Saunders, A.W. Horne: Endometriosis: new insights and opportunities for relief of symptoms, Biology of Reproduction, (in press), https://doi.org/10.1093/biolre/ioaf164
2. K. Edgley, A.W. Horne, P.T.K. Saunders, A. Tsanas: Symptom tracking in endometriosis using digital technologies: knowns, unknowns and future prospects, Cell Reports Medicine, Vol. 4(9), 101192, 2023
3. K. Edgley, P.T.K. Saunders, L.H.R. Whitaker, A.W. Horne, A. Tsanas: Insights into endometriosis symptom trajectories and assessment of surgical intervention outcomes using longitudinal actigraphy, npj Digital Medicine, Vol. 8:236, 2025
4. K. Woodward, E. Kanjo, A. Tsanas: Combining deep transfer learning with signal-image encoding for multi-modal mental wellbeing classification, ACM Transactions on Computing for Healthcare, Vol. 5(1):3, 2024 

Apply Now

Click here to Apply Now

• The deadline for 26/27 applications is Monday 12th January 2026
• Applicants must apply to a specific project. Please ensure you include details of the project on the Recruitment Form below, which you must submit to the research proposal section of your EUCLID application.
• Please ensure you upload as many of the requested documents as possible, including a CV, at the time of submitting your EUCLID application. 

Precision Medicine Recruitment Form (878.56 KB / DOCX)

Dissecting Immune-Stromal Crosstalk to Define Prognostic Endotypes in Lung Cancer

Closed for Applications  

Supervisor(s): Prof Ahsan Akram, Dr Florent Petitprez, Prof Prakash Ramachandran & Prof John Le Quesne (University of Glasgow)

Centre/Institute: Centre for Inflammation Research, Institute of Regeneration and Repair

Background

Non-small cell lung cancer (NSCLC) is a biologically and clinically heterogeneous disease, representing the majority of lung cancer diagnoses and the leading cause of cancer death worldwide. While immune checkpoint blockade has improved outcomes for some patients, a significant proportion derive little to no benefit from immunotherapy. Stratifying patients for appropriate treatment, based on biologically meaningful disease endotypes, remains an urgent challenge. This proposal aims to investigate this by integrating multidimensional clinical and molecular data to identify diagnostically, prognostically, and mechanistically relevant subgroups. 

Our work has identified prognostic associations between specific immune and stromal populations in NSCLC, including T cells, B cells, and cancer-associated fibroblasts (CAFs). However, it is clear that these cell types do not act in isolation, but rather engage in complex, context-dependent crosstalk shaped by the surrounding tumour microenvironment (TME). In particular, the canonical adenosine pathway appears to be a key modulator of this interaction, promoting local immune suppression and altering cellular positioning and function. Through a series of studies, we have demonstrated the prognostic and mechanistic relevance of this tri-directional cellular interplay. Mathieson et al. showed that CAFs expressing fibroblast activation protein and podoplanin are linked to poor clinical outcomes, likely through mechanisms involving immune exclusion and extracellular matrix remodelling. O’Connor et al. further demonstrated that CAFs can drive CXCL13 production in activated T cells via TGF-beta signalling, a pathway that influences B cell recruitment and tertiary lymphoid structure formation in a context-dependent manner. Additionally, Koppensteiner et al. found that the spatial location of CD39-positive T cells within tumours predicts differential outcomes, with their presence in tumour nests or stromal regions carrying distinct prognostic significance.  Together, these findings suggest the existence of immunologically and spatially defined NSCLC endotypes, which reflect not just the abundance of individual cell types, but the nature of their interactions. This project seeks to map and understand this cross-talk in situ, with the goal of defining novel prognostic endotypes that can guide treatment decisions and the development of novel combination strategies. The multiplex panel is being optimised for each antibody component, ensuring the student will have minimal further optimisation prior to undertaking the imaging on the TMA. 

Aims

This PhD project will investigate multi-directional immune-stromal crosstalk in NSCLC to define spatial and functional signatures associated with poor prognosis and therapy resistance. The specific aims are:

1. To image a high-dimensional 60-marker immunofluorescence (IFF) panel, for profiling immune and stromal phenotypes within a clinically annotated NSCLC tissue microarray from 350 patients
2. To perform computational and spatial analyses of T cell, B cell, and CAF cross-talk, including their relationship with adenosine pathway activation, tumour stage, radiological features, and response to therapy
3. To integrate the previous analysis with open access large-scale single-cell RNA-sequencing data to characterise populations of interest at the full transcriptome resolution.
4. To extend observation of clinical relevance of particular cell subsets by performing deconvolution of open source clinically characterised cohorts with bulk RNA-sequencing to determine associations with patients survival and response to therapeutic modalities, in particular immunotherapies.
5. To conduct focused mechanistic experiments using fresh human NSCLC tissue, including co-culture assays, tumour organoids, and precision-cut lung slices, to validate key pathways and cellular interactions identified in tissue studies

Training outcomes

The student will receive multidisciplinary training in both experimental and computational methods. This will include expertise in tissue handling, multiplexed imaging, advanced microscopy, co-culture and ex vivo lung models, and mechanistic immunology. In parallel, the student will be trained in high-dimensional image analysis, spatial imaging analysis and statistics, and clinical data integration. This project will also foster development in key areas including critical thinking, independent scientific inquiry, ethical data stewardship, and communication of complex scientific findings to both specialist and non-specialist audiences.

Working within a supportive and collaborative research environment, the student will engage with a wide range of translational researchers, clinicians, and data scientists, gaining a well-rounded education in the application of spatial biology and precision oncology to real-world clinical challenges.

References

1. Mathieson, L. et al. (2020). Cancer-associated fibroblasts expressing fibroblast activation protein and podoplanin in non-small cell lung cancer predict poor clinical outcome. British Journal of Cancer.
2. O’Connor, R. A. et al. (2023). Cancer-associated fibroblasts drive CXCL13 production in activated T cells via TGF-beta. Frontiers in Immunology.
3. Koppensteiner, L. et al. (2022). Location of CD39+ T cell subpopulations within tumors predicts differential outcomes in non-small cell lung cancer. Journal for ImmunoTherapy of Cancer.
4. Hanahan, D., and Weinberg, R. A. (2011). Hallmarks of cancer: the next generation. Cell, 144(5), 646–674.

Apply Now

Click here to Apply Now

• The deadline for 26/27 applications is Monday 12th January 2026
• Applicants must apply to a specific project. Please ensure you include details of the project on the Recruitment Form below, which you must submit to the research proposal section of your EUCLID application.
• Please ensure you upload as many of the requested documents as possible, including a CV, at the time of submitting your EUCLID application. 

Precision Medicine Recruitment Form (878.56 KB / DOCX)

Forecast: Predicting Antibiotic Resistance from Susceptibility Data

Closed for Applications  

Supervisor(s): Dr Thamarai Schneiders, Dr Andrea Weisse & Dr Simon Dewar [NHS Lothian]

Centre/Institute: Centre for Inflammation Research, Institute of Regeneration and Repair

Background

We are engaged in a continual arms race in combatting antibiotic resistance1 . It seems inevitable that the launch of any antibiotic is met with the emergence of resistance. However, the speed at which this is likely to emerge and disseminate is unknown. As such, a key challenge is being able to predict the temporal, geographic and genetic basis for resistance development for new and old antibiotics2 . Can longitudinal health data help address this question? The Atlas dataset (https://atlas-surveillance.com/login ) has curated data for almost 1M samples over a 20 year period from diagnostic labs globally. Data mining efforts from the Atlas data with cohesive outputs (eg understanding resistance emergence, transmission, geographic hotspots) have been limited. We wish to exploit this dataset to address “How can we predict the emergence of resistance based on existing global datasets on antibiotic susceptibility and genome information?”. Our approach is based on linking the susceoptibility data to bacterial genomic data thus producing the first phenotype-genotype link. In previous work (L. Jurcaga, MSc thesis, U Edinburgh 2025), we have already demonstrated that the Atlas data can be used to link trends in tigecycline (novel glycycline) resistance emergence, geographic hotspots of high rates of resistance and co-linkages to other existing or new antibiotics. As such, we wish to extend this analyses using the expanded Atlas dataset (2025), with a specific focus on pathogens posing a severe threat to human health (eg E. coli and Klebsiella pneumoniae) against new antibiotics such as cefidericol, Ceftazidime-avibactam with the following aims

Aims

1. We will utilize the Atlas susceptibility data to mine for susceptibility trends linked to isolates, antibiotics, geographic location for WHO priority pathogens E. coli and Klebsiella spp. We will investigate the dataset for statistically significant trends in resistance development and shifts in susceptibility overall and in individual countries.
2. Based on the trends and geographic locations identified in Aim 1 we will then focus on Klebsiella spp.. We will acquire temporally matched genome sequences from NCBI Bioproject to analyse genetic changes linked to alterations in susceptibility. Here, we will undertake both analyses of (1) targeted (known genes) (2) de novo (unknown) genes. The alterations in the unknown genes will be undertaken by sifting the strain pools into key epidemic lineages and undertaking either a gene presence or absence or SNP-based GWAS analyses.
3. Based on genes identified in Aim 2, we will generate a subset of these known and de novo mutations to undertake targeted antibiotic resistance evolution experiments to demonstrate alterations in susceptibility to these antibiotics.
4. We will train predictive machine learning models based on relations identified in Aim 1 to trial against a retrospective collection of bacterial samples collected from the Royal Infirmary of Edinburgh.

Training outcomes

• Ability to mine large global datasets to undertake (1)descriptive (2) quantitative and (3) statistical predictions.
• Link emerging themes from the data mining to publicy available genomic data to identify relevant mutations.
• Establish if these mutations can be biologically validated to produce relevant phenotypes in vitro.
• Apply methodologies to “real-world” samples from the Royal Infirmary of Edinburgh. 

Overall, this work is expected to provide evidence of how longitudinal susceptibility data vitally supports surveillance of antibiotic resistance trends and the emergence of known and novel resistance mechanisms.

References

1. Ho et al, Antimicrobial Resistance- A concise update, Lancet Microbe (2025)
2. Cesaro et al, Challenges and applications of artificial intelligence in Infectious Diseases and Antimicrobial Resistance, npj Antimicrobials and Resistance (2025)
3. Valavarasu V et al, Prediction of Antibiotic Resistance from Surveillance Data using Machine Learning, Sci Reports, (2025)
4. Catalan, P., et al, Seeking Patterns of Antimicrobial Resistance in Atlas, an open raw MIC database with patient metadata, Nature Communications (2022)

Apply Now

Click here to Apply Now

• The deadline for 26/27 applications is Monday 12th January 2026
• Applicants must apply to a specific project. Please ensure you include details of the project on the Recruitment Form below, which you must submit to the research proposal section of your EUCLID application.
• Please ensure you upload as many of the requested documents as possible, including a CV, at the time of submitting your EUCLID application. 

Precision Medicine Recruitment Form (878.56 KB / DOCX)

iCase: Precision Medicine for early detection and intraoperative surgery of brain cancer

Closed for Applications  

Supervisor(s): Prof Marc Vendrell & Prof Paul Brennan

Centre/Institute: Institute of Regeneration and Repair

Industrial Partner: Tocris

MRC’s iCASE awards provide students with experience of collaborative research with a non academic partner, enabling the student to spend a period of time with the non-academic partner (usually no less than three months over the lifetime of the PhD).

Students who are successfully awarded an iCASE studentship are entitled to an additional £2,500 per year as a supplement to their stipend and an annual cash contribution of at least £1,400 towards the cost of the project.  The iCase project additional funding is only secured once contracts between the industrial partner and University of Edinburgh are signed. 

Background 

Glioblastomas are one of the most common and aggressive brain cancers. Current treatments provide a mean survival of 14 months, with most tumours recurring post-resection. Optical agents to aid resection are penetrating routine clinical use but improvements are needed in both sensitivity and specificity to better identify and remove malignant cells. 

Our strategy is to harness the proteomic signatures of tumour cells to develop a molecularly-targeted approach for safer and more precise intraoperative resection of brain tumours. The ability to accomplish this has been hindered by the lack of molecular tools that retain the properties of natural peptides. We have now invented a new class of non-invasive optical agents that can be conjugated to peptides and proteins to enabling effective optical imaging and light-induced resection. 

We aim to perform a peptidomic study of patient-derived glioblastoma cell lines that will allow us to identify peptides that are highly taken up and create optical agents that will be tested fresh tumour tissue samples from surgical resections. We will finally prepare for translation of the lead compounds together with Tocris enabling us to move this technology into early phase clinical trials to provide patient benefit as quickly as possible.

Our main aim is to combine proteomics, chemistry and imaging to develop a panel of biomarkers to characterise peptidomic signatures of glioblastoma and translate them into a decision-making tool for high precision brain cancer surgery

Aims

1. We will utilize the Atlas susceptibility data to mine for susceptibility trends linked to isolates, antibiotics, geographic location for WHO priority pathogens E. coli and Klebsiella spp. We will investigate the dataset for statistically significant trends in resistance development and shifts in susceptibility overall and in individual countries.
2. Based on the trends and geographic locations identified in Aim 1 we will then focus on Klebsiella spp.. We will acquire temporally matched genome sequences from NCBI Bioproject to analyse genetic changes linked to alterations in susceptibility. Here, we will undertake both analyses of (1) targeted (known genes) (2) de novo (unknown) genes. The alterations in the unknown genes will be undertaken by sifting the strain pools into key epidemic lineages and undertaking either a gene presence or absence or SNP-based GWAS analyses.
3. Based on genes identified in Aim 2, we will generate a subset of these known and de novo mutations to undertake targeted antibiotic resistance evolution experiments to demonstrate alterations in susceptibility to these antibiotics.
4. We will train predictive machine learning models based on relations identified in Aim 1 to trial against a retrospective collection of bacterial samples collected from the Royal Infirmary of Edinburgh.

Training outcomes

Generic and transferable skills provided by the supervisory team:

• Development of an in vitro proteomic platform for the selection and optimisation of agents.
• Data analysis and management, mining skills and bioinformatics.
• Design and characterisation of light-activatable peptides.
• Cell culture, microscopy, flow cytometry, functional assays and immunohistochemistry.
• Assessment of optimal agents in ex vivo human tissues.
• Image analysis (qualitative and quantitative).
• Research ethics and health and safety skills.
• Target Product Profile based on current standard of care, health economics data and technical feasibility (with Medical Innovations Team and Tocris).
• Participation in the development of marketing strategy through competitive landscape and future emerging technologies (with EI and Tocris).
• Study IP landscape and freedom to operate. Secure emerging IP, including paper and patent writing.
• Communication skills.
• Training in GMP-compliant facilities.

Apply Now

Click here to Apply Now

• The deadline for 26/27 applications is Monday 12th January 2026
• Applicants must apply to a specific project. Please ensure you include details of the project on the Recruitment Form below, which you must submit to the research proposal section of your EUCLID application.
• Please ensure you upload as many of the requested documents as possible, including a CV, at the time of submitting your EUCLID application. 

Precision Medicine Recruitment Form (878.56 KB / DOCX)

Reprogramming lipid signalling in neutrophils for precision treatment of sepsis

Closed for Applications  

Supervisor(s): Dr Clare Muir, Prof David Dockrell, Dr Charalampos Attipa & Dr James Brewer (University of Glasgow)

Centre/Institute: The Royal (Dick) School of Veterinary Studies

Background

Sepsis is one of the leading causes of mortality around the globe and is characterised by both overwhelming infection and immune dysfunction. Neutrophils protect us from sepsis by engulfing bacteria into membrane-bound vesicles called phagosomes. However, despite the key role of neutrophils in controlling infection, it is unknown how the lipids that form the phagosome membrane change in sepsis patients and what consequences lipidomic remodelling has on cell function (e.g. bacterial killing/NET release) and shaping the overall immune response to invading micro-organisms (e.g. processing of antigen for presentation). Indeed, our recent data suggests that changes in phagosome lipids trigger a subset of neutrophil phagosomes to remain connected to the extracellular environment, with implications for phagosome fate and the overall inflammatory response to invading microorganisms. 

We therefore hypothesise that sepsis induces specific alterations in phagosome lipid signalling and that these changes may impair phagosome maturation and microbial killing. Rebalancing these lipid pathways could restore immune function and improve patient outcomes. 

Aims

Aim 1

• Define how the lipidome of neutrophil phagosomes changes during sepsis.
  • This will be achieved by feeding bacteria to neutrophils isolated from ICU sepsis patients and healthy controls. Phagosomes will then be isolated and the lipidome quantified using Liquid Chromatography-Mass Spectrometry (LC-MS). Whole-cell lipidomics will also be performed to provide a snapshot of whole-cell changes in behaviour. Samples will be taken from patients following admission to ICU and microbiology will be performed on all samples to identify the causative agent.
  • Patients will be stratified into successfully treated, intermediate response to therapy and non-responsive to treatment; thus enabling evaluation of whether phagosomal lipid signatures predict patient outcomes, supporting precision medicine stratification.
  • Phagosome maturation will be measured in parallel using established pH/ROS sensitive dyes, bacterial killing assays, antigen processing and presentation assays and immunostaining for markers of phagosome maturation (e.g. Rab5, Rab7, LAMP1).
• Correlative Light Electron Microscopy (CLEM) will define how the subcellular structure of neutrophils differs between sepsis patients and healthy controls. We hypothesise that more ‘leaky phagosomes’ will be identified in sepsis patients vs healthy controls.

Aim 2

• Investigate if changing the lipidome of neutrophil phagosomes modulates phagosome maturation in vitro.
  • Candidate lipid pathways from Aim 1 (e.g., PI3P, PI(3,5)P2, sphingolipids) will be manipulated using pharmacological modulators and the effect of changing specific lipid pathways assessed using the phagosome maturation assays defined above. 

Aim 3

• In vivo validation and translational assessment
  • Candidate lipid pathways from Aim 1 and 2 will be manipulated in zebrafish using pharmacological modulators and CRISPR/Cas9 knockout/overexpression systems.
  • Live imaging of infected zebrafish will capture in real time how changes in lipid metabolism alter how a neutrophil responds to infection- thus modelling sepsis progression in vivo. 

Training outcomes

1. Bioinformatics to integrate lipidomic and clinical data into a predictive biomarker model.
2. Develop key skills in imaging, image analysis, molecular biology and lipid analysis.
3. Work with cross-disciplinary teams (including clinicians, immunologists, imaging specialists and cell biologists) at the UoE and the UoG. 

Apply Now

Click here to Apply Now

• The deadline for 26/27 applications is Monday 12th January 2026
• Applicants must apply to a specific project. Please ensure you include details of the project on the Recruitment Form below, which you must submit to the research proposal section of your EUCLID application.
• Please ensure you upload as many of the requested documents as possible, including a CV, at the time of submitting your EUCLID application. 

Precision Medicine Recruitment Form (878.56 KB / DOCX)

Shedding light on Multiple Sclerosis: Neutrophils, Sunlight and Vitamin D

Closed for Applications  

Supervisor(s): Dr Sonja Vermeren, Prof Richard Weller, Prof Anna Williams & Dr Claudia Kutter (Karolinska Institutet)

Centre/Institute: Centre for Inflammation Research, Institute for Regeneration and Repair

Background

Multiple sclerosis (MS) is a chronic autoimmune disease without known cure that affects the central nervous system and is the primary cause of non-traumatic disability in young adults. In MS, demyelination affecting nerves in the brain and spinal cord is driven by dysregulated immune cells. Risk factors for developing MS include viral infection, genetic and environmental factors including reduced sun exposure [1]. MS incidence varies by geographical location with higher incidence rates at greater distance from the equator. Scotland has amongst the highest rates of MS in the world with 1 in 500 people affected. Sunlight results in production of vitamin D (vitD) by the body. VitD acts as immunomodulator that binds the nuclear vitD receptor (VDR) and controls gene transcription of innate and adaptive immune cells. A correlation exists between vitD deficiency and MS development/progression, yet findings to date suggest that vitD supplementation does not conclusively impact MS progression. Rather, sunlight drives vitD-dependent and -independent immune pathways and both appear to be important in MS [2]. 

Neutrophils are short-lived, highly abundant circulating immune cells in humans that are key to host damage in autoimmunity [3]. Neutrophils infiltrate active lesions in MS and in its mouse model, EAE [e.g. 4]. Inhibiting neutrophil infiltration into new lesions reduced disease onset in EAE. Genetic experiments with mice have identified that neutrophils contribute to neurodegeneration in EAE, for example by employing neutrophil extracellular traps that weaken the brain blood barrier and drive demyelination and also by undergoing changes that permit them to engage in cross-talk with B and T cells [4 and others]. Neutrophils isolated from MS patients are characterized by changes in their proteome, suggesting that functional and transcriptional changes in neutrophils occur also in MS. Neutrophils express VDR, and reports in the literature suggest vitD to have immunomodulatory, anti-inflammatory functions. However, neutrophils were only recently recognized as transcriptionally active, and their vitD (or indeed sunlight)-induced transcriptional changes have not yet been analysed in any depth. This contrasts with monocytes, B and T cells, which have already been shown to be regulated transcriptioinally by sunlight in a vitD-dependent and -independent fashion [2; unpublished results, Weller laboratory]. 

This project will address the hypothesis that neutrophils are important drivers of inflammation in MS, and that vitD/sunlight exerts important immunomodulatory functions by regulating  neutrophil transcription, and thereby also MS development and progression.

Aims

This project will 

1. examine how sunlight-driven vitD-dependent and -independent pathways regulate neutrophil transcription and functionality,
2. elucidate differentially expressed genes in MS patient neutrophils, and
3. validate key findings and integrate the data obtained to look for correlations. 

Training outcomes

This project will combine experimentation and data analysis. To examine how vitD and sunlight regulate transcription, neutrophils will be isolated from healthy Scottish volunteers in winter when sunlight is insufficient to generate vitD. Blood will be taken on three occasions (at baseline; after 4 weeks vitD supplement; after 4 weeks controlled sunbed, allowing us to differentiate between changes induced by vitD and any other effects of sunlight). Analysis of the neutrophil (bulk) transcriptome under the three conditions will be performed. In parallel, MS patient neutrophils will be analysed, comparing their transcriptome with that of neutrophils from healthy controls, complemented by some analysis of serum to ascertain vitD, and markers of neutrophil activation/inflammation. Once transcriptome analysis has been completed, experiments will be designed to validate findings (e.g., validating RNA expression on a protein level). In this way, this project provide in-depth training of a PhD student, generate novel insights and build a platform for potential future improved treatment of MS patients.

References

1. Filippi et al (2018) Multiple Sclerosis. Nat Rev Disease Primers DOI: 10.1007/s00415-021-10663-x
2. Ostkamp et al (2020) Sunlight exposure exerts immunomodulatory effects to reduce MS severity. PNAS DOI: 10.1073/pnas.2018457118
3. Bissenova et al (2022) Neutrophils in autoimmunity: when the hero becomes the villain. Clin Exp Immunol DOI: 10.1093/cei/uxac093
4. Rumble et al (2015) Neutrophil-related factors as biomarkers in EAE and MS. J Exp Med DOI: 10.1084/jem.20141015

Apply Now

Click here to Apply Now

• The deadline for 26/27 applications is Monday 12th January 2026
• Applicants must apply to a specific project. Please ensure you include details of the project on the Recruitment Form below, which you must submit to the research proposal section of your EUCLID application.
• Please ensure you upload as many of the requested documents as possible, including a CV, at the time of submitting your EUCLID application. 

Precision Medicine Recruitment Form (878.56 KB / DOCX)

Regenerative Immunology, utilising Regulatory T cells to support efficient tissue repair

Closed for Applications  

Supervisors: Dr Wei-Yu Lu (The University of Edinburgh), Prof Georgia Perona-Wright (The University of Edinburgh)

About the Project

EASTBIO (College of Medicine and Veterinary Medicine) 

Understanding the contribution of reduced niche oxygenation on haematopoiesis during healthy ageing

Closed for Applications  

Supervisors: Dr Ananda Mirchandani (The University of Edinburgh), Dr Tony Ly (The University of Dundee) 

About the Project

As we age, a common phenomenon across tissues is the loss of capillaries and capillarisation. These tiny vessels are essential for the delivery of oxygen to tissues, as oxygen can only be accessed through its passive diffusion from an area with a higher partial pressure of oxygen, to a lower one. (doi:10.14336/AD.2017.0430). The ageing bone marrow is no different to other organs in this process. A number of key changes have been observed in both the circulating cells and bone marrow composition of healthily ageing individuals. These changes include an increase in the neutrophil:lymphocyte ratio (NLR) (https://doi.org/10.1182/blood-2022-170882), as well as an increase in multipotent stem cell numbers, however the function of these stem cells appears to be defective. Importantly, these observed changes are conserved across species, including in the mouse, making the aged mouse model a useful means to understand and identify the molecular mechanisms that drive this process (doi: 10.1038/s41586-024-07238-x.). 

Data from our lab has identified some overlapping changes induced by acute hypoxia  exposure in young mice, with these ageing changes, including a skewing towards myelopoiesis and a reduction of lymphopoiesis (unpublished) raising the possibility that hypoxia itself could be an important driver of the ageing bone marrow phenotype. Healthy tissue oxygenation has been largely overlooked as an important niche factor, but less so in the bone marrow, where stem cells are known to reside in less oxygenated niches enabling them to maintain quiescence (doi: 10.1038/nature13034). 

This PhD will offer the applicant the opportunity to use mouse models and human bone marrow samples, alongside both in-vivo and ex-vivo oxygen availability manipulation systems, to dissect the contribution of reduced oxygen availability to the ageing bone marrow immune phenotype. To obtain crucial new insights, the PhD student will utilize cutting edge single cell assays that will characterize gene expression and proteome changes with spatial and temporal resolution to understand bone marrow evolution during ageing. The successful candidate will assess the interplay between niche vascularity, oxygen availability and haematopoiesis to determine the molecular mechanisms that drive the changing circulating immune landscape in healthy ageing.

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Cellular responses to fluid forces: Phases across the ages

Closed for Applications  . 

Supervisors: Dr Carsten Gram Hansen (The University of Edinburgh), Dr Tyler Shendruk (The University of Edinburgh), Dr Pierre Bagnaninchi (The University of Edinburgh) 

About the Project

Water is essential for life and the most abundant molecule in the human body, accounting for more than 50% of body weight. Around 15–20% of this is extracellular, mainly interstitial fluid. These fluids, and the hydrostatic pressures they exert, are central to cellular processes in development, inflammation, regeneration, and homeostasis. Fluid forces and phases therefore play vital roles across biology.
This project will uncover how fluids influence biological structures and functions across scales, and how ageing alters these interactions. By combining intrinsic cellular ageing with ageing-induced changes in the microenvironment, we will explore how these stressors impair cellular capacity to respond to stimuli.

Research Challenge

The key challenge is to decipher the heterogeneity in how dynamic fluids influence cells. Such parameters have been difficult to study, but recent advances now allow us to do so. We will combine bioimaging, modelling, and advanced imaging platforms to analyse dynamic cellular behaviours at single-cell resolution.

Objectives

1. Develop imaging pipelines to stratify responses to fluid dynamics.
   We will extract cellular features from confocal and label-free images, enabling classification of cell types and states under different fluidic conditions.
2. Assess responses to microenvironmental change.
   Using models of young and aged microenvironments, we will analyse how cells adapt and correlate these behaviours with genetic and proteomic profiles.
3. Integrate proteomics, modelling, and imaging to identify modular nodes

By linking molecular signatures to phenotypic features captured through bioimaging, we will identify potential targets for genetic or therapeutic intervention.

Approach

The project will be delivered through an interdisciplinary, team-based framework built around these three objectives. We will combine microfluidics, phase-change systems, bioengineering, label-free quantitative phase imaging, and high-content imaging with diverse cellular models. Experimental data will be integrated with fluid simulations to enable predictive and iterative modelling.

Training and Environment

The student will join a supportive interdisciplinary environment, gaining expertise in:

• Biomedical image analysis, omics, genome editing, and molecular biology
• High-content and label-free imaging
• Tissue culture, microfluidics, and bioengineering methods
• Programming with Python/Matlab

The training programme will prepare the candidate for a broad range of career paths in academia, industry, and beyond. They will also participate in outreach, including Science Festivals and Open Doors events, and benefit from professional development workshops offered by the Institute for Academic Development (IAD).

Research Culture

The collaborative setting of the Institute for Regeneration and Repair (IRR; CGH/PB) and the Institute for Condensed Matter and Complex Systems will provide a positive, inclusive research culture. The project’s interdisciplinary and team-focused design ensures the candidate develops both deep technical expertise and cross-disciplinary collaboration skills, equipping them for future success.

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Establish proximity labelling strategies in zebrafish to capture cellular interactions in vivo 

Closed for Applications  

Supervisors: Dr Yi Feng (The University of Edinburgh), Dr Mattias Malaguti (The University of Edinburgh)

About the Project

Unravelling the outcomes of cell–cell interactions is fundamental to understanding biological processes. The ability to visualise and track these interactions in vivo greatly enhances our capacity to dissect contact-dependent communication. Synthetic biology approaches, such as the engineered synNotch system, have been successfully applied in models including mouse and fly. Zebrafish larvae, with their translucency, provide a powerful platform for live imaging of cell–cell interactions at subcellular resolution. Using lineage-specific fluorescent reporter fish, we have observed close interactions between oncogene-expressing cells and innate immune cells in vivo and demonstrate that host innate immune cells support early tumour development. However, direct contacts and interactions between emerging oncogene-expressing cells and their immediate neighbours have not yet been visualised in vivo, despite the likelihood that these interactions influence mutant cell progression, either positively or negatively. This project aims to address this gap by generating a suite of proximity-labelling transgenic zebrafish tools including the synNotch system for live imaging of neighbouring cell interactions at tumour initiation. These tools will provide broadly applicable resources for uncovering fundamental mechanisms of cell–cell communication in both development and tumourigenesis.

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

The impact of diet-microbiome-immune interactions on intestinal function

Closed for Applications  

Supervisors: Dr Chengcan Yao (The University of Edinburgh), Dr Laura Glendinning (The University of Edinburgh), Dr Cecile Benezech (The University of Edinburgh)

About the Project

Maintenance of gut health is determined by a balance among epithelial cell function, proper immune response, and symbiotic microbiota. A disruption in this balance can result in uncontrolled pathological epithelial dysfunction and diseases such as inflammatory bowel disease (IBD) and cancer. Environmental factors and life style, such as diet, smoking, and exercise, significantly impact gut health, although the underlying mechanisms have yet to be fully elucidated. Diets, especially dietary fats, have long been known to influence the gut microbiota and, consequently, both gut resident and systemic immune responses. Metabolites of dietary fats, once digested by gut commensal bacteria, can either directly stimulate host cells or act as procurers for the generation of small molecular lipid mediators such as prostaglandins (PGs). PGs play critical physiological and pathological roles in both health and disease, for example, by mediating bone development, regulating immune cell function, and driving inflammatory responses such as fever and pain. Notably, PGs are crucial in maintaining gut epithelial homeostasis, possibly through modulating host cell function and the microbiota.

In this PhD project, we will investigate the effects of dietary fats on the modulation of intestinal health and their roles in systemic metabolic functions. The main objectives of the project include examining how dietary fats modulate the gut microbiota and intestinal immune function, the effects of the microbiota on fatty acid metabolism in intestinal cells, and the roles of fatty acid metabolites in modulating gut immune cell function. We will utilise cutting-edge immunological, pharmacological, genetic and systems biological approaches to examine the interactions among intestinal immune cells, epithelial cells and the gut microbiota in response to the consumption of dietary fatty acids. Techniques such as flow cytometry, single-cell RNA-seq, and in vitro cell culture systems will be applied for profiling intestinal immune cell and assessment of epithelial function. Microbial RNA sequencing will be used for profiling the gut microbiota and identifying functional bacterial pathways, which will be validated by manipulation (i.e. depletion and transplantation) of the microbiota. Fatty acid metabolism and PG production in immune cells will be examined through immuno-metabolic phenotyping and lipidomics. The impact of lipid mediators will also be examined using pharmacological reagents and gene-modified animals. Upon completion of this project, we expect to gain a comprehensive understanding of how dietary fatty acids interact with the gut microbiome and the host immune system, and how these interactions fundamentally regulate gut health.

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Using proteomics and informatics approaches to uncover novel host antimicrobial responses in macrophages

Closed for Applications  

Supervisors: Prof David Dockrell (The University of Edinburgh), Dr Brian McHugh (The University of Edinburgh), Dr Clark Russell (The University of Edinburgh)

Introduction

Macrophages are key innate immune cells with wide-ranging antimicrobial functions. Chronic obstructive pulmonary disease (COPD) is a progressive lung disease caused by inflammation of the small airways leading to breathlessness and frequent bacterial chest infections - COPD alveolar macrophages (AM) display faulty responses to bacteria persisting in the airway (e.g. Streptococcus pneumoniae and Haemophilus influenzae), with ineffective bacterial clearance contributing to COPD worsening. Based on our data we hypothesise that COPD alters AM mitochondrial responses to bacteria and that these impact metabolism, mitochondrial reactive oxygen species (mROS) production, and mitochondrial fission; all required for pathogen clearance – defining novel bactericidal roles for these host mechanisms will advance understanding of macrophage microbicidal activity and uncover new therapeutic targets to help circumvent antimicrobial resistance.  

Project

Aim 1: Metabolic and proteomic landscape of macrophage antimicrobial responses

A proteomics screen with an unlabelled approach (via our established collaboration with Professor Doreen Cantrell at EastBio partner University of Dundee) will be used to determine core macrophage metabolic responses to bacterial infection. Comparisons of human monocyte-derived macrophages (MDM) from COPD patients and healthy controls will determine infection-related alterations in metabolic responses at baseline and following bacterial challenge, with key findings confirmed in AM obtained from bronchoscopy. Additionally, macrophages obtained from established murine models of bacterial lung infection will be compared by proteomics in control mice versus an LPS/elastase murine model of chronic lung disease. These comparative approaches will identify candidates for further evaluation.

Aim 2: Data integration to prioritise targets for validation

Proteomics results from the human and mouse studies above will be integrated with metabolomics and transcriptomics datasets generated previously in the laboratory. This will be done in silico using meta-analysis by information content, an algorithm which integrates results from genome-scale studies to generate a single aggregated gene list, ranked based on the cumulative evidence supporting each gene. This data-driven approach will further identify and prioritise key factors in the macrophage antibacterial response that can then be targeted for validation.

Aim 3: Validation in vitro and in vivo

Factors regulating mitochondrial dynamics and metabolism in macrophages will be of interest, since mROS production is associated with mitochondrial fission. After in vitro investigation (in MDM using genetic and chemical modification), the in vivo relevance of our findings will be explored in our murine model of chronic airway disease, using relevant knock-out strains.

Overall, the student will gain experience of omics methods, informatics, and mouse infection models.
 

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Investigating how neural signalling regulates adaptive immune responses

Closed for Applications  

Supervisors: Dr Laura McCulloch (The University of Edinburgh), Dr Joy Edwards-Hicks (The University of Edinburgh)

About the Project

Increasing evidence shows that our central nervous system can interact with our immune system and modulate our immune responses. Lymphocytes, in particular, have receptors for noradrenaline, a neurotransmitter that is released by our sympathetic nervous system. Our previous investigations has shown stroke leads to excessive output of noradrenaline leading to lymphocyte death and dysregulated function, however noradrenaline signalling can also increase during periods of stress and can be dysregulated with age. This indicates a key role for noradrenaline in fine tuning our adaptive immune responses but our understanding of the impact of these signals on lymphocyte function in healthy immune responses is currently limited. We have shown using in vitro models with healthy human donor cells that noradrenaline signalling can alter lymphocyte viability, proliferation and cytokine production. We would now like to understand the importance of these signals in normal homeostatic immune responses and in ageing. This could provide us with new targets to improve vaccine responsiveness and the effective development of immunological memory.

This project will use in vivo animal studies to block or enhance noradrenaline signalling during systemic bacterial challenge to understand the role of these signals in the development of a healthy immune response. Aged animals will be used to understand how dysregulation of these pathways may impair immune responses and the development of immune memory. This will be complemented with analysis of young and aged human peripheral blood monocytes to examine noradrenaline receptor expression and responsiveness.

Training provided will cover a breadth of wet lab research techniques including: in vivo research and experimental design; immunological profiling including flow cytometry, immunostaining and image analysis; measurement of soluble mediators using muliplex ELISA; isolation of cells from tissue and blood, cell culture and ex-vivo assays; metabolic profiling including SCENITH assay and mass spectrometry. Training on data analysis including relevant image analysis software, statistical analysis including graphpad prism and R and flow cytometry analysis using FlowJo will also be provided

References:

• McCulloch L, et al (2017)  Nature communications 8:15051-15016
• Ramer-Quinn DS, et al (2000) Brain, behavior, and immunity 14:239-255.
• Sanders VM (2012) Brain, behavior, and immunity 26:195-200.
• Swanson MA et al (2001) The Journal of immunology (1950) 166:232-240
   

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Peptide-based precision anti-infectives for prophylaxis and prevention of foodborne listeriosis.

Closed for Applications  

Supervisors: Prof Jose Vazquez-Boland (The University of Edinburgh), Dr Christopher R Coxon (The University of Edinburgh)

About the Project

Listeriosis is a life-threatening foodborne infection caused by the facultative intracellular pathogen Listeria monocytogenes, which can contaminate ready-to-eat preserved by refrigeration. Listeriosis primarily affects vulnerable groups, including the elderly, pregnant women and their babies, and immunocompromised individuals. The disease is severe, manifesting as meningoencephalitis, bacteraemia, stillbirth, and neonatal sepsis. It is the leading cause of death from foodborne illness in Western countries and the third most common cause of bacterial brain infection. Current antimicrobial treatments are suboptimal, with 15–35% lethality and neurological sequelae in 14–40% of cases despite therapy. Managing exposed at-risk individuals is also challenging, as antibioprophylaxis can disrupt the microbiota and promote antibiotic resistance. New approaches are therefore needed to mitigate the risks associated with Listeria contamination in the food supply chain, prevent Listeria infection in vulnerable individuals, and improve clinical management of listeriosis. This PhD project aims to develop novel molecules usable across these three fronts, with a focus on application in the food industry.

Listeria infection depends on activation of its virulence regulator PrfA, a transcription factor that senses the host environment. PrfA function is essential for pathogenesis; its inactivation renders the bacterium harmless. This project will explore PrfA inhibition as an anti-Listeria strategy, building on the host group’s fundamental discoveries on the molecular mechanisms of PrfA regulation. The Vázquez-Boland group recently showed that PrfA’s transcriptional activity is inhibited by environmental oligopeptides, which compete with its activating cofactor, glutathione, for the same binding site. This mechanism has been characterised at atomic resolution via crystal structures of PrfA–peptide complexes.

Building on these findings, this PhD will develop peptide-based PrfA inhibitors as novel anti-Listeria agents. The project will leverages structural-functional data to design, synthesise, and evaluate these compounds in relevant experimental models, including food matrices. These innovative compounds have dual potential: (i) as Listeria-targeted food-safety additives that specifically neutralise Listeria virulence without affecting food properties; and (ii) as therapeutics to prevent or treat listeriosis without disrupting the microbiota or promoting antibiotic resistance.

This CASE-EASTBIO PhD studentship brings together the University of Edinburgh (Centre for Inflammation & Infection Research, IRR Biomedical Research Institute, EaStChem School of Chemistry) with Campden-BRI-Group, an industry leader in food safety and quality innovation. You will join a unique interdisciplinary training environment at the interface of infection biology, microbial pathogenesis, chemical biology, and medicinal chemistry while gaining valuable industrial experience in food safety, contamination control and product development.

References 

1. Koopmans, M.M., Brouwer, M.C., Vazquez-Boland, J.A. & van de Beek, D. Human listeriosis. Clin Microbiol Rev, e0006019 (2022).
2. Krypotou, E. et al. Control of bacterial virulence through the peptide signature of the Habitat. Cell Rep 26, 1815-1827 e5 (2019).
3. Hainzl, T. et al. Structural basis of promiscuous inhibition of Listeria virulence activator PrfA by oligopeptides. Cell Rep 44:115290. (2024).
    

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Decipher the immune landscape of the highly regenerative mammals – Spiny mouse (Acomys)

Closed for Applications  

Supervisors: Dr Wei-Yu Lu (The University of Edinburgh), Dr Sofia Ferreira-Gonzalez (The University of Edinburgh)

About the Project

Most mammals have limited regenerative abilities for their organs following tissue damage.  Although the stable turnover of cells is well regulated in healthy individuals, the deposition of scar tissue tends to be a consequence of tissue healing following damage. Although scar deposition is required to limit the extent of the initial insult and facilitate wound closure, it also inhibits the regeneration and reorganisation of the original tissue architecture. For example, scar deposition without hair follicles on the skin following burn injury. This principle does not only apply to external organs but also to internal organs such as the intestines and the liver.

Interestingly, some mammals have remarkable regeneration ability, mainly for adapting to the environment and living conditions. For example, naked mole rats have a different immune system and adaptation to low oxygen levels that allows them to live longer underground. Furthermore, spiny mouse can shred their skin as an anti-predatory mechanism, and the skin regrows without scar deposition. It is still unclear how the Spiny mouse has such a remarkable regeneration ability, and it is thought that the immune system may contribute to the scarless regeneration. However, this is still unclear as the field is hindered by the lack of adequate tools to study the scarless regeneration process in detail. The ability to have scarless regeneration sparks great research interests and will provide insights about how we can improve human tissue repair. Humans also have a highly regenerative organ, the liver. The liver can restore to its original mass when 70% of the liver has been resected, but this regeneration mechanism tends to fail during chronic liver injury, which can be affected by diet, lifestyle and age. The adaptive immune response plays a crucial role during chronic injuries.

We aim to study the immune landscape of the regenerative spiny mouse after liver injury and whether we can augment or fine-tune the regenerative response by manipulating the immune system, especially the adaptive immune response. By comparing the regenerative capacity of the Acomys and the scarring immune landscape in mice, we hope to identify the crucial difference in the immune system and signals that determine scar and scarless tissue repair. Eventually, the understanding of these highly regenerative organisms will provide cues for improving human health.
 

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.

EASTBIO (College of Medicine and Veterinary Medicine) 

Functional Genomics of Host Determinants in Viral Entry and Transmission

Closed for Applications  

Supervisors: Dr Richard Sloan (The University of Edinburgh), Prof Kenneth Baillie (The University of Edinburgh), Dr Finn Grey (The University of Edinburgh), Dr Rob Young (The University of Edinburgh)

About the Project

The overall aim of this project is to identify host factors that govern viral entry and cross-species transmission using the signatures of evolutionary pressure and genetic variation.
Viruses depend on host cell surface and endosomal proteins to gain entry into cells, yet many of these host determinants remain uncharacterised despite being a key step in the zoonotic transmission of virus. This project will explore how host adaptation and selective pressures have shaped viral entry pathways, identifying both established and novel genetic factors that influence infection and viral host range between species.
Our recent work combines CRISPR screen ranking with pan-mammalian positive selection analysis to pinpoint antiviral and proviral genes. Using this framework, we have already identified genes that affect influenza A virus entry and transmembrane proteins influencing SARS-CoV-2 entry. Building on these findings, this PhD will integrate comparative genomics with functional experimental validation to uncover new determinants of viral entry for a range of RNA viruses, including influenza A virus, coronaviruses and paramyxoviruses.

Specific aims:
1.    Identify and characterise known viral receptors under positive selection across mammalian genomes, testing how adaptive change affects viral binding and cell tropism.
2.    Use ontology and meta-analysis approaches to highlight cell surface and endosomal proteins not previously linked to virus entry but implicated in CRISPR screens, GWAS, or evolutionary analyses.
3.    Experimentally validate candidate factors using CRISPR sub-screens and cell-based infection assays with viral pseudotype panels to define proteins affecting viral entry and transmission potential.

Research training:
The student will gain a comprehensive training that bridges molecular biology, virology, and bioinformatics. Laboratory work will include mammalian cell culture, CRISPR-based gene editing, and infection models using pseudotyped and replication competent viruses. The student will learn to perform and interpret high-content functional assays, protein–virus interaction studies, and flow cytometry analyses.

Complementing this, the project provides computational training in comparative genomics, evolutionary analysis, and integrative data mining of CRISPR screens and genetic association datasets. Full training will be provided through project work and workshops.

Working in a collaborative environment with multiple research groups with expertise in virology, molecular genetics, and host–pathogen evolution, the student will develop a broad skill set suited to both academic and applied biological research. The project will show how viruses exploit and are constrained by the genetic diversity of their hosts and how this can drive zoonosis.

References:

1. https://www.nature.com/articles/s41586-023-06034-3
2. https://www.nature.com/articles/s41588-025-02121-5
3. https://www.nature.com/articles/s41586-023-06261-8
4. https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1012763

Funding Notes

UKRI-funded studentships are open to students worldwide and will cover tuition fees at the UK rate, plus a stipend to support living costs and an annual research grant of £5,000 for the first three years of the PhD research. The proportion of international students appointed through the EASTBIO DTP is capped at 30%.  All students must meet the eligibility criteria as outlined in the UKRI guidance on UK, EU and international candidates. This guidance should be read in conjunction with the UKRI Training Grant Terms and Conditions

Apply Now 

EASTBIO Webpage (to download the documents required for email application process, detailed below) 

• EASTBIO Application
• Equality, Diversity and Inclusion (EDI) survey
• Reference Forms can be downloaded via link above

Please send your completed EASTBIO Application Form and EDI survey along with a copy of your academic transcripts to CIR.Postgraduate@ed.ac.uk before the deadline. You should also ensure that two references have been sent to CIR.Postgraduate@ed.ac.uk by the deadline using the EASTBIO Reference Form.

For research or project-related queries, please reach out directly to the supervisors. For inquiries about the application process, contact the postgraduate administrator.

The EASTBIO team will run a series of 1-hour online sessions in November/December 2025, open to applicants who have queries about the application process. Please view EASTBIO How to Apply webpage for details. 

Unfortunately due to workload constraints, we cannot consider incomplete applications.