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10.1371/journal.pone.0260451

http://scihub22266oqcxt.onion/10.1371/journal.pone.0260451
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34813629!8610263!34813629
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suck abstract from ncbi


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pmid34813629      PLoS+One 2021 ; 16 (11): e0260451
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  • Intestinal Collinsella may mitigate infection and exacerbation of COVID-19 by producing ursodeoxycholate #MMPMID34813629
  • Hirayama M; Nishiwaki H; Hamaguchi T; Ito M; Ueyama J; Maeda T; Kashihara K; Tsuboi Y; Ohno K
  • PLoS One 2021[]; 16 (11): e0260451 PMID34813629show ga
  • The mortality rates of COVID-19 vary widely across countries, but the underlying mechanisms remain unelucidated. We aimed at the elucidation of relationship between gut microbiota and the mortality rates of COVID-19 across countries. Raw sequencing data of 16S rRNA V3-V5 regions of gut microbiota in 953 healthy subjects in ten countries were obtained from the public database. We made a generalized linear model (GLM) to predict the COVID-19 mortality rates using gut microbiota. GLM revealed that low genus Collinsella predicted high COVID-19 mortality rates with a markedly low p-value. Unsupervised clustering of gut microbiota in 953 subjects yielded five enterotypes. The mortality rates were increased from enterotypes 1 to 5, whereas the abundances of Collinsella were decreased from enterotypes 1 to 5 except for enterotype 2. Collinsella produces ursodeoxycholate. Ursodeoxycholate was previously reported to inhibit binding of SARS-CoV-2 to angiotensin-converting enzyme 2; suppress pro-inflammatory cytokines like TNF-alpha, IL-1beta, IL-2, IL-4, and IL-6; have antioxidant and anti-apoptotic effects; and increase alveolar fluid clearance in acute respiratory distress syndrome. Ursodeoxycholate produced by Collinsella may prevent COVID-19 infection and ameliorate acute respiratory distress syndrome in COVID-19 by suppressing cytokine storm syndrome.
  • |*Gastrointestinal Microbiome[MESH]
  • |Actinobacteria/*physiology[MESH]
  • |COVID-19/etiology/pathology/*prevention & control[MESH]
  • |Humans[MESH]
  • |Intestines/*microbiology[MESH]
  • |SARS-CoV-2/*physiology[MESH]


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