Cardiovascular disease (CVD) has been linked to animal-based diets, which are a major source of trimethylamine (TMA), a precursor of the proatherogenic compound trimethylamine-N-oxide (TMAO). Human gut bacteria in the genus Bilophila have genomic signatures for genetic code expansion that could enable them to metabolize both TMA and its precursors without production of TMAO. We uncovered evidence that the Bilophila demethylation pathway is actively transcribed in gut microbiomes and that animal-based diets cause Bilophila to rapidly increase in abundance. CVD occurrence and Bilophila abundance in humans were significantly negatively correlated. These data lead us to propose that Bilophila, which is commonly regarded as a pathobiont, may play a role in mitigating cardiovascular disease. Human gut microbiomes have been shown to affect the development of a myriad of disease states, but mechanistic connections between diet, health, and microbiota have been challenging to establish. The hypothesis that Bilophila reduces cardiovascular disease by circumventing TMAO production offers a clearly defined mechanism with a potential human health impact, but investigations of Bilophila cell biology and ecology will be needed to fully evaluate these ideas.

中文翻译：

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扩展的遗传密码使人类肠道细菌中的三甲胺代谢成为可能

心血管疾病 (CVD) 与动物性饮食有关，动物性饮食是三甲胺 (TMA) 的主要来源，三甲胺是致动脉粥样硬化化合物三甲胺-N-氧化物 (TMAO)的前体。嗜胆菌属中的人类肠道细菌具有遗传密码扩展的基因组特征，可以使它们代谢 TMA 及其前体而不产生 TMAO。我们发现的证据表明，嗜胆菌去甲基化途径在肠道微生物组中被积极转录，并且以动物为基础的饮食会导致嗜胆菌的丰度迅速增加。人类心血管疾病的发生与嗜胆杆菌的丰度呈显着负相关。这些数据使我们建议Bilophila，通常被认为是一种病原体，可能在减轻心血管疾病方面发挥作用。人类肠道微生物群已被证明会影响无数疾病状态的发展，但饮食、健康和微生物群之间的机制联系一直难以建立。Bilophila通过规避 TMAO 产生减少心血管疾病的假设提供了一个明确定义的机制，具有潜在的人类健康影响，但需要对Bilophila细胞生物学和生态学进行调查以充分评估这些想法。