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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-1  β   were upregulated in  H. pylori -infected AGS cells. In addition, we observed increased oxidative stress, NADPH oxidase gp91phox, CD68, caspase-1/IL-1  β  , 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.

Catechins and Sialic Acid AttenuateHelicobacter pylori-Triggered Epithelial Caspase-1 Activity and EradicateHelicobacter pyloriInfection