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Am J Physiol Gastrointest Liver Physiol 280: G525-G530, 2001;
0193-1857/01 $5.00
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Vol. 280, Issue 4, G525-G530, April 2001

THEMES
Microbes and Microbial Toxins: Paradigms for Microbial-Mucosal Interactions
IV. Helicobacter pylori strain-specific activation of signal transduction cascades related to gastric inflammation

Richard M. Peek Jr.

Division of Gastroenterology, Vanderbilt University School of Medicine, Nashville 37232; and Department of Veterans Affairs Medical Center, Nashville, Tennessee 37212

Helicobacter pylori strains that possess the cag pathogenicity island induce more severe gastritis and augment the risk of developing peptic ulcer disease and distal gastric cancer. A specific mechanism by which cag+ strains may enhance gastritis is strain-selective regulation of interleukin (IL)-8 production. On contact with gastric epithelial cells, H. pylori activates multiple signal transduction cascades that regulate IL-8 secretion, including nuclear factor-kappa B and mitogen-activated protein kinases, and these events are dependent on genes within the cag island. An independent effect of cag-mediated cellular contact is translocation and phosphorylation of H. pylori proteins within the host epithelial cell. The redundancy of intracellular signaling cascades activated by H. pylori and the divergent epithelial cell responses induced by components of the cag island may contribute to the ability of this organism to persist for decades within the gastric niche.

interleukin-8; nuclear factor-kappa B; mitogen-activated protein kinases


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