期刊
JOURNAL OF IMMUNOLOGY
卷 171, 期 8, 页码 3913-3917出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.171.8.3913
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- NIDDK NIH HHS [DK56938, DK53620, DK02469] Funding Source: Medline
Helicobacter pylori infection causes a Th1-driven mucosal immune response. Cyclooxygenase (COX)-2 is up-regulated in lamina propria mononuclear cells in H. pylori gastritis. Because COX-2 can modulate Th1/Th2 balance, we determined whether H. pylori activates COX-2 in human PBMCs, and the effect on cytokine and proliferative responses. There was significant up-regulation of COX-2 mRNA and PGE(2) release in response to H. pylori preparations. Addition of COX-2 inhibitors or an antiPGE(2)Ab resulted in a marked increase in H. pylori-stimulated IL-12 and IFN-gamma production, and a decrease in IL-10 levels. Addition of PGE(2) or cAMP, the second messenger activated by PGE(2), had the opposite effect Similarly, stimulated cell proliferation was increased by COX-2 inhibitors or anti-PGE(2)Ab, and was decreased by PGE(2). Our findings indicate that COX-2 has an immunosuppressive role in H. pylori gastritis, which may protect the mucosa from severe injury, but may also contribute to the persistence of the infection.
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