Helicobacter pylori infection is characterized by an inflammatory response in the gastric epithelium, the intensity of which appears to be type-strain specific. Infections caused by Type 1 H. pylori organisms, i.e., those expressing VacA (the cytotoxin) and CagA (the cytotoxin-associated protein), are associated with a strong polymorph mucosal infiltration in vivo, and with increased secretion of interleukin-8 by epithelial cells. The inflammatory potential of Type II strains (non-cytotoxic, VacA- and CagA-negative) is probably less pronounced. The small urease subunit, porins, and other substances produced by H. pylori show neutrophil chemotactic activities in vitro. These bacterial components promote the adhesion of polymorphs to endothelial cells and stimulate polymorphs to generate oxygen reactive metabolites. This can severely damage the gastroduodenal mucosa.