AJP - GI Add DOIs to your references at manuscript stage!
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 280: G525-G530, 2001;
0193-1857/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (16)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Peek, R. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Peek, R. M., Jr.
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


This article has been cited by other articles:


Home page
 Infect. Immun.Home page
J. L. Huff, L. M. Hansen, and J. V. Solnick
Gastric Transcription Profile of Helicobacter pylori Infection in the Rhesus Macaque
Infect. Immun., September 1, 2004; 72(9): 5216 - 5226.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
S. Ismail, M. B. Hampton, and J. I. Keenan
Helicobacter pylori Outer Membrane Vesicles Modulate Proliferation and Interleukin-8 Production by Gastric Epithelial Cells
Infect. Immun., October 1, 2003; 71(10): 5670 - 5675.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. L. Marlink, K. D. Bacon, B. C. Sheppard, H. Ashktorab, D. T. Smoot, T. L. Cover, C. W. Deveney, and M. J. Rutten
Effects of Helicobacter pylori on intracellular Ca2+ signaling in normal human gastric mucous epithelial cells
Am J Physiol Gastrointest Liver Physiol, June 9, 2003; 285(1): G163 - G176.
[Abstract] [Full Text] [PDF]

Home page
 J Antimicrob ChemotherHome page
T. Kikuchi, K. Hagiwara, Y. Honda, K. Gomi, T. Kobayashi, H. Takahashi, Y. Tokue, A. Watanabe, and T. Nukiwa
Clarithromycin suppresses lipopolysaccharide-induced interleukin-8 production by human monocytes through AP-1 and NF-{kappa}B transcription factors
J. Antimicrob. Chemother., May 1, 2002; 49(5): 745 - 755.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online