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Helicobacter pylori  is a Gram-negative pathogen that can increase the risk of stomach cancer in infected patients.  H. pylori  exploits lipid rafts to infect host cells. Infection triggers clustering of Lewis x antigen (Le x ) and integrins in lipid rafts to facilitate  H. pylori  adherence to the gastric epithelium.  H. pylori  infection can be treated with probiotics containing lactic acid bacteria that offer numerous benefits to the host while lacking the side effects associated with antibiotic therapy. Previously, we showed that the cell-free supernatant (CFS) derived from  Lactobacillus rhamnosus  JB3 (LR-JB3) at a multiplicity of infection (MOI) of 25 attenuated the pathogenicity of  H. pylori . In this study, we established a mucin model to simulate the gastric environment and to further understand the influence of mucin on the pathogenesis of  H. pylori . Porcine stomach mucin dramatically upregulated  H. pylori  virulence gene expression, including that of  babA, sabA ,  fucT, vacA, hp0499, cagA , and  cagL , as well as the adhesion and invasion ability of  H. pylori  and induced increased levels of IL-8 in infected-AGS cells. The CFS derived from LR-JB3 at a MOI of 25 reduced the expression of  H. pylori sabA, fucT , and  hp0499  in mucin, as well as that of the Le x  antigen and the α5β1 integrin in AGS cells during co-cultivation. These inhibitory effects of LR-JB3 also suppressed lipid raft clustering and attenuated Lewis antigen-dependent adherence, type IV secretion system-mediated cell contact, and lipid raft-mediated entry of VacA to host cells. In conclusion, LR-JB3 could affect  H. pylori  infection through mediating lipid raft formation of the host cells. The currently unknown cues secreted from LR-JB3 are valuable not only for treating  H. pylori  infection, but also for treating diseases that are also mediated by lipid raft signaling, such as cancer and aging-associated and neurodegenerative conditions.

Antagonistic Activities of Lactobacillus rhamnosus JB3 Against Helicobacter pylori Infection Through Lipid Raft Formation