ENHANCEMENT OF NEUTROPHIL-MEDIATED AND EOSINOPHIL-MEDIATED COMPLEMENT-DEPENDENT KILLING OF SCHISTOSOMULA OF SCHISTOSOMA-MANSONI INVITRO BY LEUKOTRIENE-B4

  • 1 January 1983
    • journal article
    • research article
    • Vol. 52  (3) , 519-527
Abstract
The ability of leukotrienes [LT] and other lipoxygenase products of arachidonic acid (AA) to influence complement-dependent killing of schistosomula of S. mansoni in vitro by human neutrophils or eosinophils was studied. These lipid mediators, which included LTB4, LTC4, LTD4, 5-HETE [5-S-hydroxy-6,8,11,14-eicosatetraenoic acid] and 5-HPETE [5-hydroperoxy-6,8,11,14-eicosatetraenoic acid] had no apparent effect by themselves, on schistosomular motility or viability. In the presence of granulocytes and fresh serum (as a source of complement) LTB4 (but not LTC4, LTD4, 5-HETE or 5-HPETE) enhanced neutrophil- and (to a much lesser extent) eosinophil-mediated, complement-dependent killing. These effects varied with the concentration of LTB4, the dilution of complement and time of incubation. The percentage of LTB4-induced enhancement obtained with neutrophils was greater than that observed with eosinophils (although the latter were obtained from patients with helminthic parasitic disease). The synthetic bacterial analog f-Met-Leu-Phe, also known to amplify complement associated granulocyte events, was comparable to LTB4 in its ability to enhance neutrophil- and eosinophil-mediated, complement-dependent killing of schistosomula. LTB4, which is released in mast cell associated reactions and promotes cell locomotion and enhancement of complement receptors in vitro, increases neutrophil- and eosinophil-mediated, complement-dependent damage of schistosomula, possibly through enhancement of [complement] C3b receptors. This may be an important amplification mechanism in IgE related immunity to migrating helminthic larvae.

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