| Summary: | Non-steroidal anti-inflammatory drugs (NSAIDs) are widely applied in the treatment of inflammation, fever and for pain relief based on its efficacy in anti-inflammatory, anti-rheumatic, analgesic, antipyretic, and anticoagulation. Moreover, the relationship between NSAIDs and immune cells is quite important since. NSAIDs can negatively regulate B cell proliferation via inhibiting prostaglandin (PG), improve the imbalance of Th1/Th2 and immunologic derangement caused by Th17 differentiation, inhibit release of TNF-α by macrophages and decrease the level of tumor necrosis factor (TNF)-α, influence inflammation via controlling other inflammatory cytokines. In addition, the mechanism may be concerned with several signal pathways including PGE2 receptor 2 (PGE2-EP2), 5-hydroxytryptamine(5-HT), glucagon-like peptide-2 (GLP-2) and nuclear factor kappa-B-interleukin-6- signal transducer and activator of transcription 3 (NF-κB-IL-6-STAT3). Thus, it is necessary to further investigate the regulation and mechanism of NSAIDs on various immunocytes, potentially provide a new strategy to optimize immune funtions under trauma and disease.
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