Interaction between Helicobacter pylori and immune response to CagA: CagA antibody may down-regulate bacterial colonization and tyrosine phosphorylation

Summary Background CagA+Helicobacter pylori strains are associated with the development of gastroduodenal diseases. H. pylori possess a type IV secretion system that is responsible for the translocation of CagA into host cells. Aim To investigate the correlation between the CagA status and the severity of histological gastritis and to analyse the tyrosine phosphorylation of CagA. Methods A total of 149 H. pylori status was determined via urine antibody to H. pylori, histological examination and serum antibody against CagA. Histological gastritis was evaluated using the updated Sydney system and scored from 0 to 3. Tyrosine phosphorylation was analysed using immunoprecipitation and immunoblotting. Results Anti-CagA titres were correlated with the severity of mononuclear cell infiltration. In contrast, mean anti-CagA in patients with grade 2 bacterial density was significantly higher than those with grade 0 (P < 0.01). Mean anti-titre in patients with grade 3 tended to be lower than that seen with grade 2. CagA tyrosine phosphorylation was significantly more common in bacteria isolated from CagA-antibody-negative patients (93%;13/14) than from CagA-antibody-positive patients (29%; 4/14, P = 0.0007). Conclusions Host–bacteria interaction is regarded as one of the important factors in the development of gastroduodenal diseases.