Recently, the incidence of autoimmune hepatitis (AIH) has gradually increased, and the disease can eventually develop into cirrhosis or even hepatoma if left untreated. AIH patients are often characterized by gut microbiota dysbiosis, but whether gut microbiota dysbiosis contributes to the progression of AIH remains unclear. In this study, we investigate the role of gut microbiota dysbiosis in the occurrence and development of AIH in mice with dextran sulfate sodium salt (DSS) induced colitis. C57BL/6J mice were randomly divided into normal group, S100-induced AIH group, and DSS+S100 group (1 % DSS in the drinking water), and the experimental cycle lasted for four weeks. We demonstrate that DSS administration aggravates hepatic inflammation and disruption of the intestinal barrier, and significantly changes the composition of gut microbiota in S100-induced AIH mice, which are mainly characterized by increased abundance of pathogenic bacteria and decreased abundance of beneficial bacteria. These results suggest that DSS administration aggravates liver injury of S100-induced AIH, which may be due to DSS induced gut microbiota dysbiosis, leading to disruption of the intestinal barrier, and then, the microbiota translocate to the liver, aggravating hepatic inflammation.

近年来，自身免疫性肝炎（AIH）的发病率逐渐上升，如果不及时治疗，最终可能发展为肝硬化甚至肝癌。AIH 患者通常以肠道菌群失调为特征，但肠道菌群失调是否会导致 AIH 的进展仍不清楚。在这项研究中，我们研究了肠道菌群失调在右旋糖酐硫酸钠（DSS）诱导的结肠炎小鼠 AIH 发生和发展中的作用。C57BL/6J小鼠随机分为正常组、S100诱导AIH组、DSS+S100组（饮水中加入1%DSS），实验周期持续4周。我们证明，DSS 给药会加重肝脏炎症和肠道屏障的破坏，并显着改变 S100 诱导的 AIH 小鼠肠道微生物群的组成，其主要特征是病原菌丰度增加和有益菌丰度减少。这些结果表明，DSS给药加重了S100诱导的AIH的肝损伤，这可能是由于DSS引起肠道菌群失调，导致肠道屏障破坏，然后菌群转移到肝脏，加重肝脏炎症。