Catechins and Sialic Acid Attenuate Helicobacter pylori-Triggered Epithelial Caspase-1 Activity and Eradicate Helicobacter pylori Infection
Authors: Hung-Chih Yang
Teh-Hong Wang
Chia-Tung Shun
Chiang-Ting Chien
Jyh-Chin Yang
John Y Kao
Journal: Evidence-based Complementary and Alternative Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: inflammasome; caspase-1; gastric epithelium; Helicobacter pylori; catechins
Affiliations: Department of Internal Medicine, Hospital and College of Medicine, National Taiwan University, Taipei 10016, Taiwan., Department of Internal Medicine, Hospital and College of Medicine, National Taiwan University, Taipei 10016, Taiwan, Department of Microbiology, Hospital and College of Medicine, National Taiwan University, Taipei 10016, Taiwan, Department of Forensic Medicine and Pathology, Hospital and College of Medicine, National Taiwan University, Taipei 10016, Taiwan, Department of Medical Research, Hospital and College of Medicine, National Taiwan University, Taipei 10016, Taiwan, Department of Life Science, National Taiwan Normal University, Taipei 11677, Taiwan, Department of Internal Medicine, Division of Gastroenterology, University of Michigan Health System, Ann Arbor, Michigan 48109-5682, USA

Abstract:  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. 

Retracted: No

PubPeer comments:
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