Complement-mediated leukocyte adherence to infective larvae of Dipetalonema viteae (Filarioidea): requirement for eosinophils or eosinophil products in effecting macrophage adherence
- PMID: 6889619
Complement-mediated leukocyte adherence to infective larvae of Dipetalonema viteae (Filarioidea): requirement for eosinophils or eosinophil products in effecting macrophage adherence
Abstract
The present study reports the existence of C-mediated adherence of eosinophils and/or macrophages to filarial infective larvae of Dipetalonema viteae. C3 molecules are present on the surface of the parasite, as shown by immunofluorescence studies. Samples of fNRS depleted of AP of complement by treatment with Zymosan A or of factor B by heating at 50 degrees C for 20 min fail to mediate cell adherence to the parasite. In contrast, fNRS inactivated for CP of complement by the chelating agent EGTA retains its activity in mediating cell adherence to the parasite. There is a significant consumption of factor B and AP of complement when infective larvae are incubated in fNHS. Consumption of C4 of the CP of complement is much lower in the same test. The adherence of macrophages cannot occur without the simultaneous presence of eosinophils, whereas eosinophils probably act alone and not in concert with macrophages. The eosinophil adherence is associated with degranulation. The damage is notably enhanced by replacing the spent eosinophil population with a newly obtained population. In the present test system, mast cells did not adhere to filarial larvae even when mast cell-rich populations were used, nor did they effect macrophage adherence when presented in association with the latter. When eosinophil-enriched cell populations containing less than 1% mast cells were used, cell adherence to filarial larvae still occurred, but the presence of 30% mast cells in such cell populations markedly increased both the rate and level of adherence. We suggest that a cell-mediated adherence and destruction dependent upon the activation of complement via AP, without a requirement for specific antibody, may represent a natural mechanism of parasite killing in a nonimmune host.
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