Host cell signaling in Helicobacter pylori infection.
Helicobacter pylori represents a highly successful human microbial pathogen that has infected approximately half of the world's population. This gram-negative microorganism colonizes the human epithelial layer in the stomach and induces a state of chronic inflammation that does not resolve the underlying infection and often leads to gastric or duodenal ulcers, or more rarely to gastric cancer. Among the reactions in H. pylori-infected epithelial cells the induction of proinflammatory cytokines, cell spreading and movement, as well as a scattered phenotype appear strictly dependent on the expression of pathogenicity island-encoded proteins in H. pylori. This review will discuss the features of the H. pylori-induced signal transduction leading to changes in host cellular function. Topics discussed comprise the signaling and the phenotypes associated with the type IV secretion system, the activation of target genes involved in gastric physiology, and putative mechanisms leading to the development of gastric cancer.
Naumann
M
M
Max-Planck-Institute for Infection Biology, Department of Molecular Biology, Berlin, Germany. naumann@mpiib-berlin.mpg.de
D004847:Epithelial Cells / Q000276:immunology* / Q000378:metabolism; D016481:Helicobacter Infections / Q000276:immunology / Q000382:microbiology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006801:Humans; D007113:Immunity, Innate; D016328:NF-kappa B / Q000378:metabolism; D015398:Signal Transduction
D016328:NF-kappa B