A possible beneficial effect of Bacteroides on faecal lipopolysaccharide activity and cardiovascular diseases
A possible beneficial effect of Bacteroides on faecal lipopolysaccharide activity and cardiovascular diseases
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DOI：
10.1038/s41598-020-69983-z
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发表时间：
2020-08
影响因子：
4.6
通讯作者：
N. Yoshida;T. Yamashita;S. Kishino;Hikaru Watanabe;K. Sasaki;D. Sasaki;Tokiko Tabata;Y. Sugiyama;N. Kitamura;Yoshihiro Saito;Takuo Emoto;Tomohiro Hayashi;Tomoya Takahashi;M. Shinohara;R. Osawa;A. Kondo;Takuji Yamada;J. Ogawa;K. Hirata
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作者：
N. Yoshida;T. Yamashita;S. Kishino;Hikaru Watanabe;K. Sasaki;D. Sasaki;Tokiko Tabata;Y. Sugiyama;N. Kitamura;Yoshihiro Saito;Takuo Emoto;Tomohiro Hayashi;Tomoya Takahashi;M. Shinohara;R. Osawa;A. Kondo;Takuji Yamada;J. Ogawa;K. Hirata
粪便脂多糖（LPS）作为解释肠道微生物群与心血管疾病（CVD）进展之间相关性的有效元素已引起关注。然而，特定肠道细菌如何促进粪便LPS水平的潜在机制仍不清楚。我们回顾性分析了92例患者的资料，发现类杆菌属的丰度与粪便LPS水平呈显著负相关。对照组中类杆菌的丰度高于CVD组。通过鲎变形细胞溶解物（LAL）试验测定，类杆菌LPS的内毒素单位显著低于大肠杆菌LPS;同样，类杆菌LPS诱导相对低水平的促炎细胞因子产生，并且不会诱导小鼠败血症。在单批发酵系统中用类杆菌益生菌发酵患者粪便样品导致类杆菌丰度显著增加，这表明可以操纵人类肠道微生物群以降低粪便LPS水平。从临床角度来看，类杆菌由于其降低的LAL活性而降低粪便LPS水平;因此，增加类杆菌丰度可能作为通过降低粪便LPS水平和抑制免疫反应来预防CVD的新治疗方法。
Faecal lipopolysaccharides (LPS) have attracted attention as potent elements to explain a correlation between the gut microbiota and cardiovascular disease (CVD) progression. However, the underlying mechanism of how specific gut bacteria contribute to faecal LPS levels remains unclear. We retrospectively analysed the data of 92 patients and found that the abundance of the genusBacteroideswas significantly and negatively correlated with faecal LPS levels. The controls showed a higher abundance ofBacteroidesthan that in the patients with CVD. The endotoxin units of theBacteroidesLPS, as determined by the limulus amoebocyte lysate (LAL) tests, were drastically lower than those of theEscherichia coliLPS; similarly, theBacteroidesLPS induced relatively low levels of pro-inflammatory cytokine production and did not induce sepsis in mice. Fermenting patient faecal samples in a single-batch fermentation system withBacteroidesprobiotics led to a significant increase in theBacteroidesabundance, suggesting that the human gut microbiota could be manipulated toward decreasing the faecal LPS levels. In the clinical perspective,Bacteroidesdecrease faecal LPS levels because of their reduced LAL activity; therefore, increasingBacteroidesabundance might serve as a novel therapeutic approach to prevent CVD via reducing faecal LPS levels and suppressing immune responses.