Molecular mechanism of inflammatory reaction induced by Helicobacter pylori lipopolysaccharides with weak endotoxic activities

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Helicobacter pylori lipopolysaccharide (LPS) shares extremely low endotoxic activity compared with typical gram-negative bacterial LPS. We found that H. pylori LPS upregulated TLR4 expression via TLR2 signaling in gastric epithelial cell lines, which express very low levels of TLR4. H. pylori LPS sensitized gastric epithelial cells to other bacterial LPS through TLR4 upregulation, and promoted gastric epithelial cell growth. These activities are suggested that H. pylori LPS is a pathogenic factor for carcinogenesis.