Analysis of the relationship between invasive capability of Helicobacter pylori and gastroduodenal diseases

Helicobacter pylori (H. pylori) may enter into host cells, maybe as a facultative intracellular pathogen. This study aims to reveal the roles of internalized H. pylon in the bacterial pathopoiesis. Transmission electron microscopy was used to observe the invasion of H. pylon. Invasion rates of H. pylon (two standard strains and 43 clinical strains) were examined by gentamicin invasion assay. The cagA, cagE and vacA genes of H. pylori were detected by PCR. The cagA 3'region (cagA-EPIYA) of each strain was sequenced. The secretion of IL-8 from AGS cells and activity of NF-kappa B induced by intracellular H. pylori were tested by ELISA and the dual-luciferase reporter assay system, respectively. It was found that H. pylon could adhere to and invade AGS cells, then continue to survive and multiply in the cytoplasm. The average invasion rate of H. pylon gastric cancer plants and that of ulcer plants were both higher than that of gastritis plants (P approximate to 0.0001). In the clinical strains, cagA, vacA and cagE were all positive; cagA-EPIYA genotypes included ABD 90.7 % (39/43) and ABBD 9.3 % (4/43), all without comparability. Notably, the average invasion rate of H. pylori vacA s1c-i1-m1b plants was higher than that of vacA s1c-i1-m2 plants (P=0.0445). In addition, the intracellular H. pylon all could induce IL-8 secretion, which was decreased after cells were pretreated with anti-beta 1-integrin antibody or SN-50 (an NF-kappa B inhibitor). The intracellular H. pylon all activated NF-kappa B, which would be inhibited after cells were pretreated with anti-beta 1-integrin antibody. These results demonstrate that H. pylori invasive ability and disease severity have a positive correlation, and this intension of invasive ability is associated with the vacA mid-region, not with cagA, cagA-EPIYA or cagE. It is possible that cagA and cagE are essential for the bacterial invasion. Internalized H. pylori can activate NF-kappa B signal pathway and induce IL-8 secretion, which suggests that H. pylori invasion may be an important strategy to play a role in the development of H. pylori associated diseases.