Butyrate attenuates intestinal inflammation in Crohn’s disease by suppressing pyroptosis of intestinal epithelial cells via the cGSA-STING-NLRP3 axis

上睑下垂 丁酸盐 炎症 克罗恩病 炎症体 免疫学 疾病 肠粘膜 医学 炎症性肠病 化学 内科学 生物化学 发酵 工程类 航空航天工程
作者
Xiaofang Xu,Zhou Huang,Zhixi Huang,Xiaodan Lv,Dan Yu Jiang,Ziqian Huang,Bing Han,Guangfu Lin,Gengfeng Liu,Shiquan Li,Junhua Fan,Xiao‐Ping Lv
出处
期刊:International Immunopharmacology [Elsevier]
卷期号:143: 113305-113305
标识
DOI:10.1016/j.intimp.2024.113305
摘要

Butyrate can strengthen the intestinal epithelial barrier. However, the mechanisms by which butyrate affects intestinal epithelial cells (IECs) pyroptosis in Crohn's disease (CD) remain unclear. In this study, we collected colonic biopsy samples from CD patients and healthy controls to assess pyroptosis levels. Our findings indicated elevated expression of pyroptosis markers in CD patients, alongside distinct morphological evidence of pyroptosis in IECs. We further investigated the effects of tributyrin on pyroptosis and the cGAS-STING pathway in a trinitrobenzene sulfonic acid-induced colitis rat model. Tributyrin significantly mitigated intestinal inflammation, reduced pathological progression, and inhibited pyroptosis and cGAS-STING pathway activation in the colitis rat model. Similarly, in an in vitro model of IECs pyroptosis, sodium butyrate inhibited pyroptosis and cGAS-STING pathway activation in HT-29 cells. Co-treatment with a cGAS-STING pathway activator and butyrate demonstrated that the activator reversed the inhibitory effects of butyrate on pyroptosis and cGAS-STING pathway activation in both the colitis rat model and HT-29 cells. Mechanistically, the cGAS-STING pathway was found to interact with NLRP3. Taken together, butyrate may mitigate intestinal inflammation in CD by suppressing cGAS-STING-NLRP3 axis-mediated IECs pyroptosis. These findings offer new insights into potential therapeutic strategies for managing CD.

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