Cytoskeletal rearrangements in gastric epithelial cells in response to Helicobacter pylori infection

Helicobacter pylori causes host epithelial cell cytoskeletal rearrangements mediated by the translocation and tyrosine phosphorylation of an outer-membrane protein, CagA, and by the vacuolating cytotoxin, VacA. However, the mechanisms by which H. pylori mediates cytoskeletal rearrangements in infected host cells need to be more clearly defined. The aim of this study was to determine the effects of H. pylori isolates from children on the architecture of host gastric epithelial cells. Gastric epithelial (AGS) cells were infected with type I (cagE(+), cagA(+), VacA(+)) H. pylori, a type II H. pylori strain (cagE(-), cagA(-), VacA(-)) or a cagE isogenic mutant. Double-labelled immune fluorescence was used to detect adherent H. pylori and the distribution of F-actin, alpha-actinin and Arp3. Both type I and type II H. pylori strains induced stress fibres in gastric epithelial cells that were not observed in uninfected cells. Type I H. pylori also induced cell elongation (hummingbird phenotype) after 4 h of infection, whereas the type II H. pylori strain did not. Less elongation occurred when AGS cells were exposed to a cagE isogenic mutant, compared with the parental strain. Confocal microscopy showed Arp3 accumulation in AGS cells infected with wild-type H. pylori, but not in response to infection with the cagE mutant. These findings indicate that type I H. pylori induce a stress fibre-like phenotype in infected gastric epithelia by a mechanism that is different from the induction of host-cell elongation. In addition to CagA and VacA, cagE also impacts on the morphology of infected gastric epithelial cells.