Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
Key Laboratory of Hubei Province for Digestive System Disease, Renmin Hospital of Wuhan University, Wuhan, China.
Front Cell Infect Microbiol. 2020 Nov 27;10:594806. doi: 10.3389/fcimb.2020.594806. eCollection 2020.
There is a growing body of evidence which suggests that intestinal microbiota, especially (), are associated with intestinal immune disease such as ulcerative colitis (UC). The mechanism by which promotes intestinal epithelial cell (IEC) death remained undefined. Here, we investigated the potential mechanisms about how aggravates IEC death in UC. We first detected the abundance of in UC tissues and analyzed its relationship with the clinical characteristics of UC. Next, we explored whether promotes intestinal epithelial cell death and . Furthermore, we extracted lipopolysaccharide (LPS) of the and examined whether exacerbates UC LPS. Our results indicated that was abundant in UC tissues and was correlated with clinical characteristics. In addition, we demonstrated that and its LPS aggravated IEC death by promoted IEC autophagy. Furthermore, autophagy inhibitors, chloroquine (CQ), 3-methyladenine (3-MA) or Atg5 silencing prevented IEC death mediated by , which suggests may contribute to UC by activating autophagic cell death. All our results uncover a vital role of in autophagic cell death and UC, giving rise to a new sight for UC therapy by inhibiting excessive IEC autophagy and autophagic cell death.
越来越多的证据表明,肠道微生物群,特别是(),与肠道免疫疾病如溃疡性结肠炎(UC)有关。促进肠道上皮细胞(IEC)死亡的机制仍未确定。在这里,我们研究了关于如何加剧 UC 中 IEC 死亡的潜在机制。我们首先检测了 UC 组织中()的丰度,并分析了其与 UC 临床特征的关系。接下来,我们探讨了是否()促进肠道上皮细胞死亡()。此外,我们提取了()的脂多糖(LPS),并检查了 LPS 是否加剧 UC。我们的结果表明,()在 UC 组织中丰富,并与临床特征相关。此外,我们证明()及其 LPS 通过促进 IEC 自噬加剧了 IEC 死亡。此外,自噬抑制剂氯喹(CQ)、3-甲基腺嘌呤(3-MA)或 Atg5 沉默可阻止()介导的 IEC 死亡,这表明()可能通过激活自噬性细胞死亡而导致 UC。我们所有的结果都揭示了()在自噬性细胞死亡和 UC 中的重要作用,为通过抑制过度的 IEC 自噬和自噬性细胞死亡来治疗 UC 提供了新的思路。