| Literature DB >> 21406172 |
Toni A Nagy1, Shannon S Allen, Lydia E Wroblewski, David K Flaherty, James C Slaughter, Guillermo Perez-Perez, Dawn A Israel, Richard M Peek.
Abstract
The host immune response directed against Helicobacter pylori is ineffective in eliminating the organism and strains harboring the cag pathogenicity island augment disease risk. Because eosinophils are a prominent component of H. pylori-induced gastritis, we investigated microbial and host mechanisms through which H. pylori regulates eosinophil migration. Our results indicate that H. pylori increases production of the chemokines CCL2, CCL5, and granulocyte-macrophage colony-stimulating factor by gastric epithelial cells and that these molecules induce eosinophil migration. These events are mediated by the cag pathogenicity island and by mitogen-activated protein kinases, suggesting that eosinophil migration orchestrated by H. pylori is regulated by a virulence-related locus.Entities:
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Year: 2011 PMID: 21406172 PMCID: PMC3078468 DOI: 10.1016/j.ajpath.2010.12.018
Source DB: PubMed Journal: Am J Pathol ISSN: 0002-9440 Impact factor: 4.307