Abstract
Abstract Background: Non-steroidal anti-inflammatory drugs (NSAIDs) are effective in reducing fever, relieving pain and inhibiting inflammation. NSAIDs function through inhibition of cyclooxygenases 1 and 2 (Cox-1 and Cox-2). Cox-1 is ubiquitously expressed, while Cox-2 expression is increased during inflammation and in malignant cells. We recently showed that Cox-2 is up-regulated in normal human B lymphocytes after activation and is required for optimal antibody synthesis. We hypothesized that ibuprofen (dual Cox-1/Cox-2 inhibitor) blunts antibody synthesis in human peripheral blood mononuclear cells (PBMC) and B lymphocytes. Methods: IgM and IgG production in anti-IgM + CpG 2395 stimulated human PBMC and B cells was detected by enzyme-linked immunosorbent assay (ELISA). B cell proliferation and viability in the presence of ibuprofen was calculated using mitochondrial dehydrogenase activity (MTT) and 3H-Thymidine incorporation assays. Results: Pharmacological concentrations of ibuprofen significantly reduced IgM and IgG synthesis in human PBMC and B lymphocytes in a dose-dependent manner. Ibuprofen had only a modest effect on B cell viability, but significantly inhibited B cell proliferation. Conclusion: Ibuprofen reduces optimal antibody synthesis in part, by decreasing B cell proliferation. Research supported by DE011390, AI071064, ES01247 grants.
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