What we really need to know is if this TMAO is normal after stroke we get better recovery. WHOM do we ask that question AND get an answer? Then how do we make TMAO normal?
Gut microbes impact stroke severity via the trimethylamine N-oxide pathway
Published:June 16, 2021DOI:https://doi.org/10.1016/j.chom.2021.05.002
Highlights
- •Gut microbial transplantation studies show stroke severity is a transmissible trait
- •The metaorganismal TMAO pathway impacts infarct size and functional impairment
- •Gut microbial CutC increases host TMAO levels, cerebral infarct size, and functional deficits
Summary
Clinical studies have demonstrated associations between circulating levels of the
gut-microbiota-derived metabolite trimethylamine-N-oxide (TMAO) and stroke incident
risk. However, a causal role of gut microbes in stroke has not yet been demonstrated.
Herein we show that gut microbes, through dietary choline and TMAO generation, directly
impact cerebral infarct size and adverse outcomes following stroke. Fecal microbial
transplantation from low- versus high-TMAO-producing human subjects into germ-free
mice shows that both TMAO generation and stroke severity are transmissible traits.
Furthermore, employing multiple murine stroke models and transplantation of defined
microbial communities with genetically engineered human commensals into germ-free
mice, we demonstrate that the microbial cutC gene (an enzymatic source of choline-to-TMA transformation) is sufficient to transmit
TMA/TMAO production, heighten cerebral infarct size, and lead to functional impairment.
We thus reveal that gut microbiota in general, specifically the metaorganismal TMAO
pathway, directly contributes to stroke severity.
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