{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Scott NA"],"funding":["NIDDK NIH HHS","Medical Research Council","National Institutes of Health","Wellcome Trust","Biotechnology and Biological Sciences Research Council"],"pagination":["eaao4755"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6548564"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(464)"],"pubmed_abstract":["Macrophages in the healthy intestine are highly specialized and usually respond to the gut microbiota without provoking an inflammatory response. A breakdown in this tolerance leads to inflammatory bowel disease (IBD), but the mechanisms by which intestinal macrophages normally become conditioned to promote microbial tolerance are unclear. Strong epidemiological evidence linking disruption of the gut microbiota by antibiotic use early in life to IBD indicates an important role for the gut microbiota in modulating intestinal immunity. Here, we show that antibiotic use causes intestinal macrophages to become hyperresponsive to bacterial stimulation, producing excess inflammatory cytokines. Re-exposure of antibiotic-treated mice to conventional microbiota induced a long-term, macrophage-depen"],"journal":["Science translational medicine"],"pubmed_title":["Antibiotics induce sustained dysregulation of intestinal T cell immunity by perturbing macrophage homeostasis."],"pmcid":["PMC6548564"],"funding_grant_id":["100290/Z/12/Z","097820/Z/11/B","206206/Z/17/Z","MR/N023625/1","MR/K021095/1","MR/M00242X/1","BBS/E/F/000PR10356","203128","T32-DK07632","BB/J004529/1","206206","BBS/E/F/000PR10353","BBS/E/F/00044409","100974/C/13/Z","R01GM108527","203128/Z/16/Z","BB/R003114/1","1R21AI097419","T32 DK007632","100974"],"pubmed_authors":["Wessel H","Leclaire C","Thomson CA","Alcon-Giner C","Connolly JPR","Caim S","Andersen P","Milling SWF","Mowat AM","Hall LJ","Andrusaite A","Lawson M","Wang P","Shaw T","Roe AJ","Travis MA","Bravo-Blas A","Mann ER","Kastele V","Grencis R","Le Gall G","Peterson DA","Li X","Scott NA","Bancroft A"],"additional_accession":[]},"is_claimable":false,"name":"Antibiotics induce sustained dysregulation of intestinal T cell immunity by perturbing macrophage homeostasis.","description":"Macrophages in the healthy intestine are highly specialized and usually respond to the gut microbiota without provoking an inflammatory response. A breakdown in this tolerance leads to inflammatory bowel disease (IBD), but the mechanisms by which intestinal macrophages normally become conditioned to promote microbial tolerance are unclear. Strong epidemiological evidence linking disruption of the gut microbiota by antibiotic use early in life to IBD indicates an important role for the gut microbiota in modulating intestinal immunity. Here, we show that antibiotic use causes intestinal macrophages to become hyperresponsive to bacterial stimulation, producing excess inflammatory cytokines. Re-exposure of antibiotic-treated mice to conventional microbiota induced a long-term, macrophage-depen","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Oct","modification":"2026-05-07T08:15:43.111Z","creation":"2019-07-24T07:09:41Z"},"accession":"S-EPMC6548564","cross_references":{"pubmed":["30355800"],"doi":["10.1126/scitranslmed.aao4755"]}}