التفاصيل البيبلوغرافية
| العنوان: |
Effects of cyclooxygenase-1 and -2 gene disruption on Helicobacter pylori-induced gastric inflammation. |
| المؤلفون: |
Li GQ, Xia HH, Chen MH, Gu Q, Wang JD, Peng JZ, Chan AO, Cho CH, So HL, Lam SK, Hu PJ, Liang YJ, Lin HL, Berg DE, Feng ZH, Langenbach R, Wong BC |
| المصدر: |
Journal of Infectious Diseases; 4/1/2006, Vol. 193 Issue 7, p1037-1046, 10p |
| مستخلص: |
BACKGROUND: Cyclooxygenases (COXs) play important roles in inflammation and carcinogenesis. The present study aimed to determine the effects of COX-1 and COX-2 gene disruption on Helicobacter pylori-induced gastric inflammation. METHODS: Wild-type (WT), COX-1 and COX-2 heterozygous (COX-[1+/-] and COX-2[+/-]), and homozygous COX-deficient (COX-1[-/-] and COX-2[-/-]) mice were inoculated with H. pylori strain TN2 and killed after 24 weeks of infection. Uninfected WT and COX-deficient mice were used as controls. Levels of gastric mucosal inflammation, epithelial cell proliferation and apoptosis, and cytokine expression were determined. RESULTS: COX deficiency facilitated H. pylori-induced gastritis. In the presence of H. pylori infection, apoptosis was increased in both WT and COX-deficient mice, whereas cell proliferation was increased in WT and COX-1-deficient, but not in COX-2-deficient, mice. Tumor necrosis factor (TNF)-alpha and interleukin-10 mRNA expression was elevated in H. pylori-infected mice, but only TNF-alpha mRNA expression was further increased by COX deficiency. Prostaglandin E2 levels were increased in infected WT and COX-2-deficient mice but were at very low levels in infected COX-1-deficient mice. Leukotriene (LT) B[4] and LTC[4] levels were increased to a similar extent in infected WT and COX-deficient mice. CONCLUSIONS: COX deficiency enhances H. pylori-induced gastritis, probably via TNF-alpha expression. COX-2, but not COX-1, deficiency suppresses H. pylori-induced cell proliferation. Copyright © 2006 Infectious Diseases Society of America [ABSTRACT FROM AUTHOR] |
|
Copyright of Journal of Infectious Diseases is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder