The microbial metabolite desaminotyrosine protects from influenza through type I interferon

Posted by: | August 8, 2017 | Comments


Eat more plants for influenza resilience
Antibiotic treatment worsens influenza in mice, possibly because the concomitant loss of the microbiota interrupts the production of bioactive metabolites. Steed et al. found that a microbial product, desaminotyrosine (DAT), produced by an obligate clostridial anaerobe from the digestion of plant flavonoids, is beneficial during influenza. DAT enters the bloodstream and triggers type I interferon signaling, which then augments antiviral responses by phagocytic cells. Without DAT, influenza virus causes inflammation and severe disease.

Science, this issue p. 498

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.

Check Out More: Science | AAAS

Ashley L. Steed, George P. Christophi, Gerard E. Kaiko3 Lulu Sun, Victoria M. Goodwin, Umang Jain3 Ekaterina Esaulova, Maxim N. Artyomov, David J. Morales, Michael J. Holtzman, Adrianus C. M. Boon, Deborah J. Lenschow, Thaddeus S. Stappenbeck. Science 04 Aug 2017: Vol. 357, Issue 6350, pp. 498-502. DOI: 10.1126/science.aam5336

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