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Helicobacter pylori  infection is associated with several gastrointestinal disorders in the human population worldwide. High-mobility group box 1 (HMGB1), a ubiquitous nuclear protein, mediates various inflammation functions. The interaction between HMGB1 and receptor for advanced glycation end-products (RAGE) triggers nuclear factor (NF)-κB expression, which in turn stimulates the release of proinflammatory cytokines, such as interleukin (IL)-8, and enhances the inflammatory response. However, how  H. pylori  activates HMGB1 expression and mobilizes RAGE into cholesterol-rich microdomains in gastric epithelial cells to promote inflammation has not been explored. In this study, we found that HMGB1 and RAGE expression increased significantly in  H. pylori -infected cells compared with -uninfected cells. Blocking HMGB1 by neutralizing antibody abrogated  H. pylori -elicited RAGE, suggesting that RAGE expression follows HMGB1 production, and silenced RAGE-attenuated  H. pylori -mediated NF-κB activation and IL-8 production. Furthermore, significantly more RAGE was present in detergent-resistant membranes extracted from  H. pylori -infected cells than in those from -uninfected cells, indicating that  H. pylori  exploited cholesterol to induce the HMGB1 signaling pathway. These results indicate that HMGB1 plays a crucial role in  H. pylori -induced inflammation in gastric epithelial cells, which may be valuable in developing treatments for  H. pylori -associated diseases.

Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells