Complex cellular responses of Helicobacter pylori-colonized gastric adenocarcinoma cells. Infect Immun 2011; 79:2362–71

Helicobacter pylori is an important class I carcinogen that persistently infects the human gastric mucosa to induce gastritis, gastric ulceration, and gastric cancer. H. pylori pathogenesis strongly depends on pathogenic factors, such as VacA (vacuolating cytotoxin A) or a specialized type IV secretion system (T4SS), which injects the oncoprotein CagA (cytotoxin-associated gene A product) into the host cell. Since access to primary gastric epithelial cells is limited, many studies on the complex cellular and molecular mechanisms of H. pylori were performed in immortalized epithelial cells originating from individual human adenocarcinomas. The aim of our study was a comparative analysis of 14 different human gastric epithelial cell lines after colonization with H. pylori. We found remarkable differences in host cell morphology, extent of CagA tyrosine phosphorylation, adhesion to host cells, vacuolization, and interleukin-8 (IL-8) secretion. These data might help in the selection of suitable cell lines to study host cell responses to H. pylori in vitro, and they imply that different host cell factors are involved in the determination of H. pylori pathogenesis. A better understanding of H. pylori-directed cellular responses can provide novel and more balanced insights into the molecular mechanisms of H. pylori-dependent pathogenesis in vivo and may lead to new therapeutic approaches. Helicobacter pylori has been identified as the causative agent associated with inducing inflammatory disorders, in