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 di scharges from patients with Trichomonas vaginalis infection. In this s tudy, we investigated the effect of humoral immunity on leukotriene B4 (LTB4) generation by neutrophils in the inflammatory response of vagi nal trichomoniasis. As quantitated by a radioimmunoassay, no release o f LTB4 was detected from neutrophils (5 x 10(6)/ml) interacted with tr ichomonads (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, augm ented LTB4 production (1 . 4 +/- 0 . 4 ng/ml, n = 5) by neutrophils, s uggesting that this enhancement is Fc gamma receptor-mediated. Moreove r, addition of the specific IgG (1 mg/ml) to C2-deficient serum or Fac tor B-deficient serum, but not C5-deficient serum, significantly incre ased LTB4 production by neutrophils in response to trichomonad stimula tion. This indicates that the complement common pathway activation is crucial for the amplification of host defence mechanisms against T. va ginalis. An LTB4 receptor antagonist, SC-41930, completely abolished n eutrophil chemotactic activity induced by LTB4. Taken together, these results indicate that humoral immunity could promote the interaction o f neutrophils with T. vaginalis and augment the inflammatory response through the amplification of LTB4 production.