Open AccessComplex Cellular Responses of Helicobacter pylori-Colonized Gastric Adenocarcinoma Cells
Author(s) -
Sabine Schneider,
Gert Carra,
Uğur Şahin,
Benjamin Hoy,
Gabriele Rieder,
Silja Weßler
Publication year - 2011
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.01350-10
Subject(s) - helicobacter pylori , biology , adenocarcinoma , helicobacter infections , spirillaceae , gastric adenocarcinoma , helicobacter , microbiology and biotechnology , gastritis , immunology , cancer , genetics
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 ofH. 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 withH. 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 toH. pylori in vitro , and they imply that different host cell factors are involved in the determination ofH. pylori pathogenesis. A better understanding ofH. pylori -directed cellular responses can provide novel and more balanced insights into the molecular mechanisms ofH. pylori -dependent pathogenesisin vivo and may lead to new therapeutic approaches.