tetano
Editor, Senior Moderator
Science. 2017 Aug 4;357(6350):498-502. doi: 10.1126/science.aam5336.
[h=1]The microbial metabolite desaminotyrosine protects from influenza through type I interferon.[/h] Steed AL[SUP]1,[/SUP][SUP]2[/SUP], Christophi GP[SUP]3,[/SUP][SUP]2[/SUP], Kaiko GE[SUP]2[/SUP], Sun L[SUP]2[/SUP], Goodwin VM[SUP]1,[/SUP][SUP]2[/SUP], Jain U[SUP]2[/SUP], Esaulova E[SUP]2,[/SUP][SUP]4[/SUP], Artyomov MN[SUP]2[/SUP], Morales DJ[SUP]3,[/SUP][SUP]2[/SUP], Holtzman MJ[SUP]3[/SUP], Boon ACM[SUP]3,[/SUP][SUP]2,[/SUP][SUP]5[/SUP], Lenschow DJ[SUP]3,[/SUP][SUP]2[/SUP], Stappenbeck TS[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
Copyright ? 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
PMID: 28774928 DOI: 10.1126/science.aam5336
[h=1]The microbial metabolite desaminotyrosine protects from influenza through type I interferon.[/h] Steed AL[SUP]1,[/SUP][SUP]2[/SUP], Christophi GP[SUP]3,[/SUP][SUP]2[/SUP], Kaiko GE[SUP]2[/SUP], Sun L[SUP]2[/SUP], Goodwin VM[SUP]1,[/SUP][SUP]2[/SUP], Jain U[SUP]2[/SUP], Esaulova E[SUP]2,[/SUP][SUP]4[/SUP], Artyomov MN[SUP]2[/SUP], Morales DJ[SUP]3,[/SUP][SUP]2[/SUP], Holtzman MJ[SUP]3[/SUP], Boon ACM[SUP]3,[/SUP][SUP]2,[/SUP][SUP]5[/SUP], Lenschow DJ[SUP]3,[/SUP][SUP]2[/SUP], Stappenbeck TS[SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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.
Copyright ? 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
PMID: 28774928 DOI: 10.1126/science.aam5336