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Helicobacter pylori is a unique microorganism capable of long-term colonization of the gastric mucosa, induction of the inflammatory process, antigenic mimicry and immune evasia. Flagella proteins, adhesins, invasive and aggressive enzymes, cytotoxin-associated protein, vacuolating cytotoxin can have a damaging effect on stomach epithelial cells. Recognition of molecular patterns of Helicobacter pylori by stomach cell receptors initiates activation of adapter proteins, protein kinases and transcription factors, leading to the production of proinflammatory cytokines, infiltration by neutrophilic granulocytes, absorption and killing of microorganisms by phagocytes with presentation of antigens to lymphocytes, while the activity and completeness of phagocytosis remain at a low level. Activation of CD8+-, CD16+- lymphocytes is accompanied by cytotoxic effect on both Helicobacter pylori and epithelial cells of the gastric mucosa. Weak immunogenicity of Helicobacter pylori antigens limits the production of anti-Helicobacter antibodies. Thus, activation of immune factors, in most cases, does not lead to complete elimination of the pathogen, but can aggravate the pathomorphological changes of the gastric epithelium.

Significance of pathogenicity factors in initiation of immune response in Helicobacter pylori infection