Dapsone inhibits LTB4 binding and bioresponse at the cellular and physiologic levels

Radioligand binding studies using human neutrophils exposed to 10-100 microM dapsone indicated that this anti-inflammatory compound antagonized association of LTB4 (leukotriene B4) with its specific receptor sites. Binding inhibition was manifested in reduced biologic response of the neutrophils as determined in LTB4-stimulated chemotaxis. In addition, a physiologic model of LTB4-dependent inflammation in mice was antagonized by systemic administration of dapsone. These data suggest that inhibition of LTB4 binding may represent the cellular mechanism of action responsible for the anti-inflammatory effects of dapsone.