Cutting edge: cyclooxygenase-2 activation suppresses Th1 polarization in response to Helicobacter pylori.

Meyer F, Ramanujam KS, Gobert AP, James SP, Wilson KT
J Immunol. 2003 171 (8): 3913-7

PMID: 14530307 · DOI:10.4049/jimmunol.171.8.3913

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 anti-PGE(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.

MeSH Terms (19)

Cells, Cultured Cyclic AMP Cyclooxygenase 2 Dinoprostone Down-Regulation Enzyme Activation Growth Inhibitors Helicobacter pylori Humans Interferon-gamma Interleukin-10 Interleukin-12 Isoenzymes Leukocytes, Mononuclear Membrane Proteins Prostaglandin-Endoperoxide Synthases Th1 Cells Th2 Cells Up-Regulation

Connections (1)

This publication is referenced by other Labnodes entities:

Links