This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Loh, J. T. Articles by Cover, T. L. Search for Related Content PubMed Articles by Loh, J. T. Articles by Cover, T. L.

Regulation of Helicobacter pylori cagA Expression in Response to Salt

Departments of ¹ Medicine and ² Microbiology and Immunology, Vanderbilt University Medical Center; ³ Veterans Affairs Tennessee Valley Healthcare System, Nashville, Tennessee

Requests for reprints: Timothy L. Cover, Division of Infectious Diseases, Vanderbilt University School of Medicine, A2200 Medical Center North, Nashville, TN 37232. Phone: 615-322-2035; E-mail: timothy.L.cover{at}vanderbilt.edu.

Helicobacter pylori infection and a high dietary salt intake are risk factors for the development of gastric adenocarcinoma. In this study, we tested the hypothesis that high salt concentrations might alter gene expression in H. pylori. Transcriptional profiling experiments indicated that the expression of multiple H. pylori genes, including cagA, was regulated in response to the concentrations of sodium chloride present in the bacterial culture medium. Increased expression of cagA in response to high salt conditions was confirmed by the use of transcriptional reporter strains and by immunoblotting. H. pylori CagA is translocated into gastric epithelial cells via a type IV secretion pathway, and on entry into target cells, CagA undergoes tyrosine phosphorylation and causes multiple cellular alterations. Coculture of gastric epithelial cells with H. pylori grown under high salt conditions resulted in increased tyrosine-phosphorylated CagA and increased secretion of interleukin-8 by the epithelial cells compared with coculture of the cells with H. pylori grown under low salt conditions. Up-regulation of H. pylori cagA expression in response to high salt concentrations may be a factor that contributes to the development of gastric adenocarcinoma. [Cancer Res 2007;67(10):4709–15]

This article has been cited by other articles:

				R. M. Peek Jr Review: Prevention of gastric cancer: When is treatment of Helicobacter pylori warranted? Therapeutic Advances in Gastroenterology, July 1, 2008; 1(1): 19 - 31. [Abstract] [PDF]

				H. Gancz, K. R. Jones, and D. S. Merrell Sodium Chloride Affects Helicobacter pylori Growth and Gene Expression J. Bacteriol., June 1, 2008; 190(11): 4100 - 4105. [Abstract] [Full Text] [PDF]