{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Duffin R"],"funding":["CREST","BLRD VA","VA Merit Award","GlaxoSmithKline","Chief Scientists Office","NIH","European Union FP7","University of Edinburgh","NIDDK NIH HHS","Medical Research Council","Chief Scientist Office","National Institute for Health Research (NIHR)","Health Foundation/Academy of Medical Sciences","Wellcome Trust","Biotechnology and Biological Sciences Research Council","Rainin Trust","MRC UK","Wellcome Trust Institutional Strategic Support Fund"],"pagination":["1333-8"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4841390"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["351(6279)"],"pubmed_abstract":["Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic i"],"journal":["Science (New York, N.Y.)"],"pubmed_title":["Prostaglandin E₂ constrains systemic inflammation through an innate lymphoid cell-IL-22 axis."],"pmcid":["PMC4841390"],"funding_grant_id":["G0601481","106122","13H6","BB/K091121/1","DK37097","I01 BX000616","MR/K013386/1","MR/L012766/1","106122/A/14/Z","CL-2015-14-002","ETM202","R01 DK037097","MR/K017047/1","BB/K019112/1","ETM/202","G1000868","1BX000616","G0901697"],"pubmed_authors":["Pellicoro A","Narumiya S","Rossi F","Mole DJ","Iredale JP","Zheng X","Forster T","Crittenden S","O'Connor RA","Richards J","Howie SE","Maizels RM","Rossi AG","Duffin R","Robb CT","Anderton SM","Smyth D","Ghazal P","Yu C","Skouras C","Breyer RM","Tang S","Yao C","Weller RB"],"additional_accession":[]},"is_claimable":false,"name":"Prostaglandin E₂ constrains systemic inflammation through an innate lymphoid cell-IL-22 axis.","description":"Systemic inflammation, which results from the massive release of proinflammatory molecules into the circulatory system, is a major risk factor for severe illness, but the precise mechanisms underlying its control are not fully understood. We observed that prostaglandin E2 (PGE2), through its receptor EP4, is down-regulated in human systemic inflammatory disease. Mice with reduced PGE2 synthesis develop systemic inflammation, associated with translocation of gut bacteria, which can be prevented by treatment with EP4 agonists. Mechanistically, we demonstrate that PGE2-EP4 signaling acts directly on type 3 innate lymphoid cells (ILCs), promoting their homeostasis and driving them to produce interleukin-22 (IL-22). Disruption of the ILC-IL-22 axis impairs PGE2-mediated inhibition of systemic i","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Mar","modification":"2026-05-05T07:01:17.81Z","creation":"2019-03-27T02:12:13Z"},"accession":"S-EPMC4841390","cross_references":{"pubmed":["26989254"],"doi":["10.1126/science.aad9903"]}}