Catechins and Sialic Acid AttenuateHelicobacter pylori-Triggered Epithelial Caspase-1 Activity and EradicateHelicobacter pyloriInfection
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 duringHelicobacter pyloriinfection is yet to be elucidated. Here, we investigated the effect of catechins (CAs), sialic acid (SA), or combination of CA and SA (CASA) onH. pylori-induced caspase-1-mediated epithelial damage, as well asH. pyloricolonizationin vitro(AGS cells) andin vivo(BALB/c mice). Our results indicate that the activity of caspase-1 and the expression of its downstream substrate IL-1βwere upregulated inH. 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 ofH. pylori-infected mice. We have further demonstrated that treatment with CASA led to synergistic anti-H. pyloriactivity and was more effective than treatment with CA or SA alone. In particular, treatment with CASA for 10 days eradicatedH. pyloriinfection in up to 95% ofH. pylori-infected mice. Taken together, we suggest that the pathogenesis ofH. pyloriinvolves a gastric epithelial inflammasome/caspase-1 signaling pathway, and our results show that CASA was able to attenuate this pathway and effectively eradicateH. pyloriinfection.