Ultrastructural and immunological aspects of the phagocytosis of Trypanosoma brucei by mouse peritoneal macrophages.
Trypanosome-activated mouse peritoneal macrophages phagocytized and digested Trypanosoma brucei in vitro and in vivo, but in the absence of specific antiserum and complement the degree of phagocytosis was minimal. Ultrastructurally, the parasites attached to the macrophage by their flagella, and ingestion proceeded flagellum first. Once ingested, T. brucei was degraded, presumably due to fusion of the parasite-containing phagosome with lysosomes. Contrariwise, normal mouse peritoneal macrophages displayed negligible ability to ingest T. brucei, even in the presence of specific antiserum and complement. During trypanosomiasis in deer mice (Peromyscus maniculatus), the development of hypergammaglobulinemia correlated with enhanced phagocytosis of T. brucei by macrophages, but only at early post-inoculation days (PID 5 to 15). Complement lysis of trypanosomes was not identified in these experiments. Between PID 20 to 30, antiserum and complement either had no phagocytosis-promoting ability or depressed the phagocytosis of T. brucei by macrophages. These results indicate that both specific antibody and complement contribute to the ingestion of T. brucei by activated macrophages, but that parasite antigenic variation effectively abrogates the phagocytic defense mechanism.
D000818:Animals; D000906:Antibodies; D001202:Ascitic Fluid / Q000166:cytology; D003165:Complement System Proteins / Q000378:metabolism; D005260:Female; D008264:Macrophages / Q000276:immunology / Q000502:physiology* / Q000648:ultrastructure; D008297:Male; D010542:Peromyscus; D010587:Phagocytosis; D014346:Trypanosoma brucei brucei / Q000276:immunology*
D000906:Antibodies; D003165:Complement System Proteins