期刊
SCIENCE
卷 357, 期 6350, 页码 498-502出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aam5336
关键词
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资金
- Pediatric Scientist Development Program
- National Institute of Child Health and Human Development, NIH [5K12HD000850-30, T32 DK007130-43]
- NIAID [U19-AI070412, R01-AI111605]
- Crohn's and Colitis Foundation/Helmsley Charitable Trust
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, Clostridium orbiscindens, 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 effects on responses to lethal infections through modulation of type I IFN.
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