{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Steed AL"],"funding":["NICHD NIH HHS","NIDDK NIH HHS","NIAID NIH HHS","NHLBI NIH HHS","Crohn’s Colitis"],"pagination":["498-502"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5753406"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["357(6350)"],"pubmed_abstract":["The microbiota is known to modulate the host response to influenza infection through as-yet-unclear mechanisms. We hypothesized that components of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analysis of influenza in a gain-of-function genetic mouse model. Here we show that a microbially associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of type I IFN signaling and diminution of lung immunopathology. A specific human-associated gut microbe, <i>Clostridium orbiscindens,</i> produced DAT and rescued antibiotic-treated influenza-infected mice. DAT protected the host by priming the amplification loop of type I IFN signaling. These findings show that specific components of the enteric microbiota have distal effe"],"journal":["Science (New York, N.Y.)"],"pubmed_title":["The microbial metabolite desaminotyrosine protects from influenza through type I interferon."],"pmcid":["PMC5753406"],"funding_grant_id":["R01 AI111605","T32 DK007130","U19 AI070412","U19 AI070489","K12 HD000850","UH3 HL123429","award312855","P30 DK056341","R01 AI130591"],"pubmed_authors":["Steed AL","Stappenbeck TS","Christophi GP","Esaulova E","Morales DJ","Sun L","Artyomov MN","Lenschow DJ","Holtzman MJ","Goodwin VM","Kaiko GE","Jain U","Boon ACM"],"additional_accession":[]},"is_claimable":false,"name":"The microbial metabolite desaminotyrosine protects from influenza through type I interferon.","description":"The microbiota is known to modulate the host response to influenza infection through as-yet-unclear mechanisms. We hypothesized that components of the microbiota exert effects through type I interferon (IFN), a hypothesis supported by analysis of influenza in a gain-of-function genetic mouse model. Here we show that a microbially associated metabolite, desaminotyrosine (DAT), protects from influenza through augmentation of type I IFN signaling and diminution of lung immunopathology. A specific human-associated gut microbe, <i>Clostridium orbiscindens,</i> produced DAT and rescued antibiotic-treated influenza-infected mice. DAT protected the host by priming the amplification loop of type I IFN signaling. These findings show that specific components of the enteric microbiota have distal effe","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Aug","modification":"2025-04-03T23:18:23.27Z","creation":"2019-03-27T03:06:22Z"},"accession":"S-EPMC5753406","cross_references":{"pubmed":["28774928"],"doi":["10.1126/science.aam5336"]}}