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• W2103159301 abstract "BackgroundCyclooxygenases (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 MethodsWild-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 ResultsCOX 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)–α and interleukin–10 mRNA expression was elevated in H. pylori–infected mice, but only TNF-α 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) B4 and LTC4 levels were increased to a similar extent in infected WT and COX-deficient mice ConclusionsCOX deficiency enhances H. pylori–induced gastritis, probably via TNF-α expression. COX-2, but not COX-1, deficiency suppresses H. pylori–induced cell proliferation" @default.
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• W2103159301 date "2006-04-01" @default.
• W2103159301 modified "2023-10-18" @default.
• W2103159301 title "Effects of Cyclooxygenase‐1 and ‐2 Gene Disruption on<i>Helicobacter pylori</i>–Induced Gastric Inflammation" @default.
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• W2103159301 doi "https://doi.org/10.1086/500984" @default.
• W2103159301 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16518767" @default.
• W2103159301 hasPublicationYear "2006" @default.
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