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4,4`-diaminodiphenyl sulfone (dapsone) is a sulfone drug that has antibacterial effects on a variety of bacteria, especially Mycobacterium leprae; thus, it has been used to treat leprosy. Previous studies demonstrated that dapsone inhibits integrin-mediated adherence of neutrophils and production of prostaglandin by polymorphonuclear leukocytes. Hence, dapsone may act in immune cells and regulate cell-mediated inflammation processes. However, its anti-inflammatory effects remain unclear. The present study demonstrated that dapsone modulates the production of inflammation-related cytokines in immune cells. We employed the spleen cells of mice, which are major immune cells, and lipopolysaccharide (LPS) as a causative agent of inflammation for experiments. Dapsone induced a proportional change in splenocyte subsets and the apoptosis of spleen cells. Interestingly, dapsone decreased the production of tumor necrosis factor-alpha and interleukin (IL)-10, but not IL-6, in LPS-treated spleen cells. In other assays, we measured the dapsone-induced production of nitric oxide (NO) and the expression of activation markers of spleen cells. Dapsone decreased NO production in LPS-treated spleen cells. Taken together, our results demonstrate that dapsone has anti-inflammatory effects in immune cells and provide new insight into the potential uses of this agent.

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Anti-inflammatory effects of 4,4'-diaminodiphenyl sulfone (dapsone) in lipopolysaccharide-treated spleen cells: selective inhibition of inflammation-related cytokines