Studies suggest that host cell signal transduction cascades are manipulated
during infection with microbes, including the gastric pathogen Helicobacte
r pylori. Several putative adhesins have been proposed to mediate the attac
hment of H pylori to gastric epithelial cells. Following bacterial binding,
a series of signalling pathways are activated in the infected gastric epit
helial cell. These signals include both cytoplasmic (such as vacuolization,
tyrosine phosphorylation and elevation of cytosolic calcium) and nuclear (
proliferation, apoptosis and chemokine transcription) events. Research aime
d at elucidating the interactions that occur between the host cell and the
bacterium during infection should improve the limited knowledge of disease
pathogenesis.