is a major aetiological agent in gastroduodenal disorders and adherence of the bacteria to the gastric mucosa is one of the initial stages of infection. Although a number of specific adhesins has been identified, other virulence factors may play a role in adherence to gastric epithelial cells directly or through interaction with other adhesins. This study assessed the effect of 16 virulence factors on the adherence of the bacteria to gastric AGS cells and on gastric epithelial cell cycle distribution. Defined isogenic SS1 mutants were used. After co-incubation of gastric AGS cells and bacteria, adherence of to AGS cells was visualised by immunofluorescence microscopy and quantified by flow cytometry. Cell cycle phase distribution was analysed by flow cytometry with propidium iodide staining. Mutants were tested for their ability to adhere to AGS cells and compared with the wild-type SS1 strain. Mutations in genes in the pathogenicity island showed that and mutants adhered less than the wild-type strain to AGS cells, whereas a mutant showed no reduction in adherence. Mutations in genes involved in flagellar biosynthesis showed that the adherence ability of , and mutants was reduced, but a mutant possessed wild-type levels of adherence. Mutations in genes coding for the urease () and phospholipase () enzymes did not affect adherence, but mutation of the gene encoding an haemolysin resulted in a reduced adherence. A mutant, with reduced adherence to AGS cells, was less able to induce AGS cell apoptosis than SS1. The ability to induce GG cell cycle arrest was also abolished in the mutant. However, an increased cell number in S phase was observed when AGS cells were exposed to the mutant compared with SS1, suggesting that unattached bacteria may still be able to stimulate cell proliferation. In addition to known adhesins, other bacterial virulence factors such as CagE, CagP, FliQ, FliM, FliS and TlyA appear to play a role in adherence to gastric epithelial cells. Mutations in these genes may affect pathogenicity by reducing either the ability of the bacteria to attach to gastric epithelial cells or the intensity of bacteria–host cell interactions.


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