Catechins and sialic acid attenuate helicobacter pylori -triggered epithelial caspase-1 activity and eradicate helicobacter pylori infection

Jyh Chin Yang, Hung Chih Yang, Chia Tung Shun, Teh Hong Wang, Chiang Ting Chien*, John Y. Kao

*此作品的通信作者

研究成果: 雜誌貢獻期刊論文同行評審

25 引文 斯高帕斯(Scopus)

摘要

The inflammasome/caspase-1 signaling pathway in immune cells plays a critical role in bacterial pathogenesis; however, the regulation of this pathway in the gastric epithelium during Helicobacter pylori infection is yet to be elucidated. Here, we investigated the effect of catechins (CAs), sialic acid (SA), or combination of CA and SA (CASA) on H. pylori-induced caspase-1-mediated epithelial damage, as well as H. pylori colonization in vitro (AGS cells) and in vivo (BALB/c mice). Our results indicate that the activity of caspase-1 and the expression of its downstream substrate IL-1β were upregulated in H. pylori-infected AGS cells. In addition, we observed increased oxidative stress, NADPH oxidase gp91phox, CD68, caspase-1/IL-1β, and apoptosis, but decreased autophagy, in the gastric mucosa of H. pylori-infected mice. We have further demonstrated that treatment with CASA led to synergistic anti-H. pylori activity and was more effective than treatment with CA or SA alone. In particular, treatment with CASA for 10 days eradicated H. pylori infection in up to 95% of H. pylori-infected mice. Taken together, we suggest that the pathogenesis of H. pylori involves a gastric epithelial inflammasome/caspase-1 signaling pathway, and our results show that CASA was able to attenuate this pathway and effectively eradicate H. pylori infection.

原文英語
文章編號248585
期刊Evidence-based Complementary and Alternative Medicine
2013
DOIs
出版狀態已發佈 - 2013

ASJC Scopus subject areas

  • 補充和替代醫學

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