Complement component C1q enhances invasion of human mononuclear phagocytes and fibroblasts by Trypanosoma cruzi trypomastigotes.

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Abstract
Internalization and infectivity of Trypanosoma cruzi trypomastigotes by macrophages is enhanced by prior treatment of parasites with normal human serum. Heating serum or removing Clq from serum abrogates the enhancement, but augmentation of attachment and infectivity is restored by addition of purified serum source. Although both noninfective epimastigotes (Epi) and vertebrate-stage tissue culture trypomastigotes (TCT) bind Clq in saturable fashion at 4.degree. C, internalization by monocytes and macrophages of TCT but not Epi-bearing Clq is enhanced in comparison to untreated parasites. Adherence of human monocytes and macrophages to surfaces coated with Clq also induce a marked enhancement of the internalization of native TCT. Clq enhances attachment of both Epi and TCT to human foreskin fibroblasts, but only when Clq is on the parasite and not when the fibroblasts are plated on Clq-coated surfaces. Only TCT coated with Clq show enhanced invasion into fibroblasts. Although trypomastigotes produce an inhibitor of the complement cascade which limits C3 deposition during incubation in normal human serum, Clq binds to the parasite and enhances entry of trypomastigotes into target cells.