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Microbial Transplantation With Human Gut Commensals Containing CutC Is Sufficient to Transmit Enhanced Platelet

Sarah M Skye1,2, Weifei Zhu1,2, Kymberleigh A Romano1,2,3

  • 1From the Department of Cellular and Molecular Medicine, Lerner Research Institute (S.M.S., W.Z., K.A.R., Z.W., X.J., J.K., B.H., J.A.D., W.H.W.T., S.L.H.), Cleveland Clinic, OH.

Circulation Research
|October 26, 2018
PubMed
Abstract

Insights

The gut microbial cutC gene drives trimethylamine (TMA) production, increasing TMA-derived trimethylamine N-oxide (TMAO) levels. This microbial pathway enhances platelet reactivity and thrombosis risk, offering a target for heart disease treatment.

Area of Science:

  • Microbiology
  • Cardiovascular Science
  • Metabolomics

Background:

  • Gut microbes significantly impact cardiovascular disease and thrombosis risk via trimethylamine N-oxide (TMAO) production.
  • Microbial generation of trimethylamine (TMA), the TMAO precursor, is a critical, rate-limiting step in this pathway.
  • Specific microbial enzymes, like choline TMA-lyases encoded by cutC/D genes, catalyze TMA production in human commensals.

Purpose of the Study:

  • To demonstrate that the gut microbial cutC gene is sufficient to transmit enhanced platelet reactivity and thrombosis potential to a host.
  • To investigate the role of microbial cutC-dependent TMA/TMAO production in vivo.

Main Methods:

  • Utilized gnotobiotic mice and microbial colonization studies.
  • Compared thrombosis potential in germ-free mice colonized with high TMA-producing human fecal communities versus a defined CutC-deficient community.
  • Examined the effect of a CutC-expressing commensal and its isogenic ΔcutC mutant (Clostridium sporogenes Δ cutC).

Main Results:

  • Microbial cutC-dependent TMA/TMAO production was sufficient to transmit heightened platelet reactivity and thrombosis potential to the host.
  • Colonization studies confirmed the direct link between microbial cutC activity and increased thrombosis risk.

Conclusions:

  • The microbial choline TMA-lyase pathway, specifically involving the cutC gene, is a key mediator of TMA/TMAO-driven thrombosis.
  • This pathway represents a rational molecular target for therapeutic intervention in atherothrombotic heart disease.
Keywords:
cardiovascular diseasesgastrointestinal microbiomehumansmetabolismthrombosis

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