Schistosoma mansoni: loss of the ability of schistosomula to bind mouse complement following intravenous injection into mice.
The ability of freshly prepared schistosomula to become opsonized by the alternative pathway of mouse complement in vivo was investigated. Skin schistosomula were intravenously injected into mice and recovered shortly afterwards from their lungs. Following an in vivo residency of a few minutes, most schistosomula had considerably less C3b detectable by immunofluorescence on their surface than worms which had been incubated for the same time with mouse serum in vitro. Deposition of C3b was undetectable on all schistosomula following an in vivo residency of a few hours. Irradiation or treatment with puromycin of the schistosomula prior to injection did not alter the difference between in vitro and in vivo complement deposition. Moreover, schistosomula which had been passaged briefly through a mouse, lost most of their ability to deposit mouse complement on their surface during a subsequent in vitro incubation with mouse serum. It is suggested that opsonization of freshly transformed schistosomula with C3b of murine complement is less efficient in vivo than in vitro.
D000818:Animals; D003167:Complement Activation; D003179:Complement C3b / Q000378:metabolism*; D003170:Complement Pathway, Alternative; D005455:Fluorescent Antibody Technique; D008168:Lung / Q000469:parasitology; D008297:Male; D051379:Mice; D011223:Praziquantel / Q000494:pharmacology; D014176:Protein Biosynthesis; D011691:Puromycin / Q000494:pharmacology; D012550:Schistosoma mansoni / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism
D011691:Puromycin; D011223:Praziquantel; D003179:Complement C3b