Influence of humoral immunity on leukotriene B4 production by neutrophils in response to Trichomonas vaginalis stimulation.

Neutrophils are the predominant inflammatory cells found in vaginal discharges from patients with Trichomonas vaginalis infection. In this study, we investigated the effect of humoral immunity on leukotriene B4 (LTB4) generation by neutrophils in the inflammatory response of vaginal trichomoniasis. As quantitated by a radioimmunoassay, no release of LTB4 was detected from neutrophils (5 x 10(6)/ml) interacted with trichomonads (1 x 10(6)/ml). However, specific immunoglobulin G(IgG) but not F(ab')2, at a titre of 1:256 directed against T. vaginalis, augmented LTB4 production (1.4 +/- 0.4 ng/ml, n = 5) by neutrophils, suggesting that this enhancement is Fc gamma receptor-mediated. Moreover, addition of the specific IgG (1 mg/ml) to C2-deficient serum or Factor B-deficient serum, but not C5-deficient serum, significantly increased LTB4 production by neutrophils in response to trichomonad stimulation. This indicates that the complement common pathway activation is crucial for the amplification of host defence mechanisms against T. vaginalis. An LTB4 receptor antagonist, SC-41930, completely abolished neutrophil chemotactic activity induced by LTB4. Taken together, these results indicate that humoral immunity could promote the interaction of neutrophils with T. vaginalis and augment the inflammatory response through the amplification of LTB4 production.