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Статья
The microbial metabolite desaminotyrosine protects from influenza through type I interferon
2021
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. © 2017, American Association for the Advancement of Science. All rights reserved.
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Версии
- 1. Version of Record от 2021-04-27
Метаданные
Название журнала
- Science
Том
- 357
Выпуск
- 6350
Страницы
- 498-502
Ключевые слова
- desaminotyrosine; interferon; type i interferon; unclassified drug; guanine nucleotide binding protein; Ifi1 protein, mouse; interferon; phenylpropionic acid derivative; phloretic acid; antibiotics; bacterium; digestive system; influenza; metabolite; protein; animal experiment; animal model; animal tissue; Article; Clostridium; Clostridium orbiscindens; controlled study; experimental influenza; gain of function mutation; gene amplification; host; immunomodulation; immunopathology; intestine flora; metabolite; mouse; nonhuman; priority journal; signal transduction; animal; cell line; Clostridium perfringens; genetics; host pathogen interaction; immunology; intestine flora; knockout mouse; lung; metabolism; orthomyxovirus infection; Clostridium orbiscindens; Mus; Animals; Cell Line; Clostridium perfringens; Gastrointestinal Microbiome; GTP-Binding Proteins; Host-Pathogen Interactions; Interferon Type I; Lung; Mice; Mice, Knockout; Orthomyxoviridae Infections; Phenylpropionates; Signal Transduction
Издатель
- American Association for the Advancement of Science
Тип документа
- journal article
Источник
- scopus
