Статья

The microbial metabolite desaminotyrosine protects from influenza through type I interferon

A. Steed, G. Christophi, G. Kaiko, L. Sun, V. Goodwin, U. Jain, E. Esaulova, M. Artyomov, D. Morales, M. Holtzman, A. Boon, D. Lenschow, T. Stappenbeck,
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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  • 1. Version of Record от 2021-04-27

Метаданные

Об авторах
  • A. Steed
    Department of Pediatrics, Washington University, School of Medicine, St. Louis, MO 63110, United States
  • G. Christophi
    Department of Medicine, Washington University, School of Medicine, St. Louis, MO 63110, United States
  • G. Kaiko
    Department of Pathology and Immunology, Washington University, School of Medicine, St. Louis, MO 63110, United States
  • L. Sun
    Computer Technologies Department, Saint Petersburg National Research University of Information Technologies, Mechanics and Optics, Saint Petersburg, 197101, Russian Federation
  • V. Goodwin
    Department of Molecular Microbiology, Washington University, School of Medicine, St. Louis, MO 63110, United States
  • U. Jain
  • E. Esaulova
  • M. Artyomov
  • D. Morales
  • M. Holtzman
  • A. Boon
  • D. Lenschow
  • T. Stappenbeck
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