H. pylori is a causative agent of chronic gastritis. Gastrointestinal disorders are associated with a bacterial mechanism of adaptation to the stomach's environment and the immune responses of gastric epithelial cells. The efficacy of H. pylori lipopolysaccharides identify cation by host cells is determined by their chemical structure. This paper focuses mainly on the molecular mechanisms of innate immune evasion by H. pylori, the Toll-like receptor 2/4 activity of epithelial and immune system cells, and molecular mimicry (Lewis antigen).