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Regulation of the growth and differentiation of Trypanosoma (Trypanozoon) brucei brucei in resistant (C57B1/6) and susceptible (C3H/He) mice
Author(s) -
BLACK S.J.,
SENDASHONGA C.N.,
LALOR P.A.,
WHITELAW D.D.,
JACK R.M.,
MORRISON W.I.,
MURRAY M.
Publication year - 1983
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1983.tb00761.x
Subject(s) - trypanosoma brucei , biology , parasite hosting , antibody , immune system , spleen , antigen , trypanosomiasis , virology , ratón , immunology , biochemistry , world wide web , gene , computer science
Summary While Trypanosoma brucei brucei GUTat 3 were equally infective for C3H/Heand for C57B1/6 mice at doses ranging from 5 to 5 × 10 3 organisms and had similar prepatent periods in both strains of mice, infected C57B1/6 mice displayed lower parasitaemia, shorter times to parasite wave remission and survived for a longer time than infected C3H/He mice. Parasite growth and differentiation rates and host immune responses were similar for the first 5 days in both strains of mice after infection with 10 3 T.b.brucei GUTat 3 but, thereafter, parasite differentiation proceeded more rapidly and specific antibodies reached higher titres in C57B1/6 than in C3H/He mice. In contrast, parasite growth and differentiation rates were similar in irradiated mice of both strains. Furthermore, following inoculation of intact mice with irradiated T.b.brucei GUTat 3, C3H/Hemice actually mounted higher titred antibody responses than C57B1/6 mice showing that they were not intrinsically defective in their capacity to respond to GUTat 3 antigens. Parasite differentiation occurred at the same rate in irradiated (650r) C57B1/6 mice and in irradiated C57B1/6 mice reconstituted with syngeneic spleen cells although T.b.brucei GUTat 3 specific antibody was detected in the latter mice prior to peak parasitaemia. Furthermore, it was shown directly in C57B1/6 mice that there was no selective destruction of slender form T.b.brucei GUTat 3 parasites during the phase of accumulation of stumpy form parasites. These studies indicate that the more rapid differentiation of T.b.brucei GUTat 3 parasites in infected C57B1/6 mice as compared to infected C3H/Hemice was unlikely to be directly related to the more efficient antibody response in the infected C57B1/6 mice. The observations suggest that there might be an association between host mechanisms which regulate differentiation of T.b.brucei parasites and those which regulate antibody responses.