“Cag PAI HAVE A FUNCTION RELATED WITH ADHESION TO GASTRIC EPITHELIAL CELLS”

Abstract

ObjectiveThe cag pathogenecity island (PAI) is a major virulence factor of Helicobacter pylori (H.p). Andherent ability of H. pylori to the gastric epithelial cells is an important initial step for bacterial virulance. The hpaA and bab A2 genes are thought to be major adherent‐associated genes. Some of cag genes have partial homology to the flagellar aparatus or other adhesion related gene. It is not fully investigated whether cag PAI is related with the adherent ability to the gastric epithelial cells. To evaluate the interaction between the structure of Cag PAI and adherent ability to the gastric epithelial cells.MethodsThe polymerase chain reaction (PCR) and Southern blot analysis were used to determine the structure of cag PAI in Japanese 236 clinical isolates. The PCR and Southern blot analysis were used to verity the presence or absence of hpaA and bab A2. Adherent ability H. pylori to the gastric epithelial cells (KATO cells) was examined in the tested strains by flow‐cytometric analysis (FACS) using anti‐H. pylori antibody.ResultsSeven cag PAI partial deleted strains of tested 236 strains (3.0%) were found by PCR and southern blot analysis, and which showed 3 pattern in deleted region within cag PAI. All cagG‐deleted strains showed less ability of adhesion than CagG positive strains. The peak counts of the cells adhered with cagG deleted strains ( n = 4 ) were significantly lower than that of cagG positive strains ( n = 8 ) ( mean peak count ± SE ; 27.3 ± 2.9 vs 54.8 ± 4.9 ) by FACS analysis. All of cagG‐deleted strains posessed hpaA gene. Six of them possesed babA2 gene.ConclusionsOur results demonstrated that cagG‐deleted clinical isolates had less ability of adhesion to the gastric epithelial cells, even if hpaA and babA2 gene are present.