Gut microbiota in PSC : From association to possible causality. Commentary to “Gut pathobionts underlie intestinal barrier dysfunction and liver T helper 17 cell immune response in primary sclerosing cholangitis” by Nakamoto et al., Nature Microbiology, January 2019 - INRAE - Institut national de recherche pour l’agriculture, l’alimentation et l’environnement Accéder directement au contenu
Article Dans Une Revue Clinics and Research in Hepatology and Gastroenterology Année : 2020

Gut microbiota in PSC : From association to possible causality. Commentary to “Gut pathobionts underlie intestinal barrier dysfunction and liver T helper 17 cell immune response in primary sclerosing cholangitis” by Nakamoto et al., Nature Microbiology, January 2019

Résumé

Primary sclerosing cholangitis is a chronic cholestatic liver disease, whose pathogenesis remains poorly understood. Several studies have shown that PSC patients harbor an impaired gut microbiota. A recent study confirmed that PSC patients displayed a bacterial dysbiosis, characterized by an increased abundance of three different bacteria: Klebsiella pneumoniae, Proteus mirabilis and Enterococcus gallinarum. This study also provides evidence for a possible mechanism of action of these bacteria: notably the formation of pores in gut epithelium leading to an increased gut permeability and the induction of liver inflammation characterized by an increased proportion of T helper 17 (T(H)17) cells. For the first time, strong data demonstrate not only an association between gut microbiota and primary sclerosing cholangitis but also a possible causal link.

Dates et versions

hal-02945772 , version 1 (22-09-2020)

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Sara Lemoinne, Joao Sabino, Harry Sokol. Gut microbiota in PSC : From association to possible causality. Commentary to “Gut pathobionts underlie intestinal barrier dysfunction and liver T helper 17 cell immune response in primary sclerosing cholangitis” by Nakamoto et al., Nature Microbiology, January 2019. Clinics and Research in Hepatology and Gastroenterology, 2020, 44 (2), pp.123-125. ⟨10.1016/j.clinre.2019.06.005⟩. ⟨hal-02945772⟩
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