{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Dore E"],"funding":["Natural Sciences and Engineering Research Council of Canada"],"pagination":["e152638"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8855825"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(2)"],"pubmed_abstract":["Secreted phospholipase A2-IIA (sPLA2-IIA) hydrolyzes phospholipids to liberate lysophospholipids and fatty acids. Given its poor activity toward eukaryotic cell membranes, its role in the generation of proinflammatory lipid mediators is unclear. Conversely, sPLA2-IIA efficiently hydrolyzes bacterial membranes. Here, we show that sPLA2-IIA affects the immune system by acting on the intestinal microbial flora. Using mice overexpressing transgene-driven human sPLA2-IIA, we found that the intestinal microbiota was critical for both induction of an immune phenotype and promotion of inflammatory arthritis. The expression of sPLA2-IIA led to alterations of the intestinal microbiota composition, but housing in a more stringent pathogen-free facility revealed that its expression could affect the im"],"journal":["JCI insight"],"pubmed_title":["The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammation."],"pmcid":["PMC8855825"],"funding_grant_id":["RGPIN-2016-05830"],"pubmed_authors":["Rangachari M","Davidovic L","Cloutier N","Boilard E","Morozumi S","Allaeys I","Duchez AC","Payre C","Arita M","Martin C","Joly-Beauparlant C","Flamand N","Droit A","Bodein A","Petit-Paitel A","Levesque T","Lambeau G","Gelb MH","Murakami M","Dore E","Mathieu A","Leclercq M"],"additional_accession":[]},"is_claimable":false,"name":"The interaction of secreted phospholipase A2-IIA with the microbiota alters its lipidome and promotes inflammation.","description":"Secreted phospholipase A2-IIA (sPLA2-IIA) hydrolyzes phospholipids to liberate lysophospholipids and fatty acids. Given its poor activity toward eukaryotic cell membranes, its role in the generation of proinflammatory lipid mediators is unclear. Conversely, sPLA2-IIA efficiently hydrolyzes bacterial membranes. Here, we show that sPLA2-IIA affects the immune system by acting on the intestinal microbial flora. Using mice overexpressing transgene-driven human sPLA2-IIA, we found that the intestinal microbiota was critical for both induction of an immune phenotype and promotion of inflammatory arthritis. The expression of sPLA2-IIA led to alterations of the intestinal microbiota composition, but housing in a more stringent pathogen-free facility revealed that its expression could affect the im","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2026-05-30T23:54:54.471Z","creation":"2025-04-04T23:29:06.051Z"},"accession":"S-EPMC8855825","cross_references":{"pubmed":["35076027"],"doi":["10.1172/jci.insight.152638"]}}