1887

Abstract

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 mediates cytoskeletal rearrangements in infected host cells need to be more clearly defined. The aim of this study was to determine the effects of isolates from children on the architecture of host gastric epithelial cells. Gastric epithelial (AGS) cells were infected with type I ( , , VacA) , a type II strain ( , , VacA) or a isogenic mutant. Double-labelled immune fluorescence was used to detect adherent and the distribution of F-actin, α-actinin and Arp3. Both type I and type II strains induced stress fibres in gastric epithelial cells that were not observed in uninfected cells. Type I also induced cell elongation (hummingbird phenotype) after 4 h of infection, whereas the type II strain did not. Less elongation occurred when AGS cells were exposed to a isogenic mutant, compared with the parental strain. Confocal microscopy showed Arp3 accumulation in AGS cells infected with wild-type , but not in response to infection with the mutant. These findings indicate that type I 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, also impacts on the morphology of infected gastric epithelial cells.

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2003-10-01
2024-12-07
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