Helicobacter pylori-induced epithelial cell signalling in gastric carcinogenesis.
Helicobacter pylori represents a highly successful human microbial pathogen that infects the stomach of more than half of the world's population. H. pylori induces gastric inflammation, and the diseases that can follow such infection include chronic gastritis, peptic ulcers and, more rarely, gastric cancer. The reasons why a minority of patients with H. pylori develops gastric cancer could be related to differences in host susceptibility, environmental factors and the genetic diversity of the organism. This review examines the features of H. pylori-induced epithelial cell signalling in gastric diseases. Clinical studies and animal models, and also evidence for H. pylori strain-related differences in gastric epithelial cell proliferation in vivo are discussed. In addition, the mechanisms by which H. pylori triggers hyperproliferative processes and takes direct command of epithelial cell signalling, including activation of tyrosine kinase receptors, cell-cell interactions and cell motility are reviewed.
Naumann
Michael
M
Experimental Internal Medicine, Medical Faculty, Otto-von-Guericke-University, 39120 Magdeburg, Germany.
Crabtree
Jean E
JE
D000818:Animals; D002455:Cell Division; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000382:microbiology* / Q000502:physiology*; D016481:Helicobacter Infections / Q000382:microbiology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D051379:Mice; D015398:Signal Transduction; D013274:Stomach Neoplasms / Q000382:microbiology / Q000503:physiopathology*