Human eosinophil- and neutrophil-mediated killing of schistosomula of <i>Schistosoma mansoni in vitro</i>. I. Enhancement of complement-dependent damage by mast cell-derived mediators and formyl methionyl peptides.

Abstract

Abstract Mast cell-associated chemical mediators (histamine and the ECF-A tetrapeptides (Val-Gly-Ser-Glu and Ala-Gly-Ser-Glu)), agents previously shown to enhance complement (C) receptors on human eosinophils, were tested for their capacity to influence C-dependent killing of schistosomula of Schistosoma mansoni. The valyl- and alanyl- ECF-A tetrapeptides, and histamine, increased eosinophil-mediated C-dependent killing of schistosomula in a dose- and time-dependent fashion. These agents had no apparent influence on eosinophil-mediated antibody-dependent schistosomula death or (with the valylpeptide) on neutrophil-mediated C-dependent killing of schistosomula. Similarly, several formyl methionyl peptides, including F-Met-Leu-Phe, F-Met-Met-Phe, and F-Met-Phe, enhanced neutrophil-mediated C-dependent killing of schistosomula in a comparable fashion to that achieved by mast cell-derived mediators and eosinophils. These results indicate that certain pharmacologic agents, particularly those that promote cell locomotion in vitro, increase C-dependent damage of schistosomula, presumably through enhancement of C3b receptors, and that this may be an important amplification mechanism in immunity to migrating helminthic larvae.