The microbial metabolite desaminotyrosine protects from influenza through type I interferon
Ashley Steed(Washington University in St. Louis), George P. Christophi(Washington University in St. Louis), Gerard E. Kaiko(Washington University in St. Louis), Lulu Sun(Washington University in St. Louis), Victoria M. Goodwin(Washington University in St. Louis), Umang Jain(Washington University in St. Louis), Ekaterina Esaulova(Washington University in St. Louis), Maxim N. Artyomov(Washington University in St. Louis), David J. Morales(Washington University in St. Louis), Michael J. Holtzman(Washington University in St. Louis), Adrianus C. M. Boon(Washington University in St. Louis), Deborah J. Lenschow(Washington University in St. Louis), Thaddeus S. Stappenbeck(Washington University in St. Louis)
Cited by 587Open Access
Abstract
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
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