John Savill's aim is to understand mechanisms by which myeloid phagocyte clearance of cells dying by apoptosis serves to suppress inflammatory responses, both during resolution of inflammation and the endogenous suppression of inflammation threatened by "commensal" bacteria. Professor Sir John Savill Chair of Experimental Medicine Centre for Inflammation Research Contact details Phone: +44 (0)131 242 6587 Website: Academic Profile Email: john.savill@ed.ac.uk Group MembersAiliang Zhang - Research AssistantBackgroundAimsTo understand mechanisms by which myeloid phagocyte clearance of cells dying by apoptosis serves to suppress inflammatory responses, both during resolution of inflammation and the endogenous suppression of inflammation threatened by "commensal" bacteria. BackgroundThe group has a longstanding interest in mechanisms of apoptotic cell clearance by phagocytes, focusing in particular on the role of the myeloid alpha-v integrin family. The fundamental hypothesis is that "phagocyte clearance determines the meaning of cell death".Approaches and ProgressThe main focus at the moment is to exploit availability of the Cre-directed deletion of alpha-v in myeloid cells. A key feature of the work is collaboration with Dr Adam Lacy-Hulbert, Principal Investigator at the Benaroya Research Institute in Seattle.Research OverviewIn healthy tissues, unwanted cells are usually deleted by a programme of natural cell death (apoptosis), which leads to rapid clearance of intact dying cells by scavenger cells, particularly bone marrow-derived macrophages and dendritic cells (the latter evolved specifically to control immune responses by interaction with cells of the T lymphocyte family). These mechanisms are known to be important in resolution of inflammation, where large numbers of white blood cells can be deleted by the processes of apoptosis and swift phagocytosis, and there is also evidence that defects in these processes can contribute to chronic inflammation. More recently, however, our work has emphasised that the clearance of dying cells from both the gut and the lung may in fact maintain an anti-inflammatory and immunosuppressive micro-environment in these organs, which serves to prevent commensal bacteria from inciting inflammation. Go to the Edinburgh Research Explorer Sources of FundingMedical Research CouncilMore information on funding at John Savill's Research Explorer profile. This article was published on 2024-09-10