Regulation of the growth and differentiation of Trypanosoma (Trypanozoon) brucei brucei in resistant (C57B1/6) and susceptible (C3H/He) mice

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cg.identifier.doihttps://doi.org/10.1111/j.1365-3024.1983.tb00761.xen
cg.issn0141-9838en
cg.issue5en
cg.journalParasite Immunologyen
cg.subject.ilriANIMAL DISEASESen
cg.subject.ilriLIVESTOCKen
cg.subject.ilriDISEASE CONTROLen
cg.volume5en
dc.contributor.authorBlack, Samuel J.en
dc.contributor.authorSendashoga, Cyrie N.en
dc.contributor.authorLalor, P.A.en
dc.contributor.authorWhitelaw, D.D.en
dc.contributor.authorJack, R.M.en
dc.contributor.authorMorrison, W. Ivanen
dc.contributor.authorMurray, M.en
dc.date.accessioned2013-06-11T09:23:18Zen
dc.date.available2013-06-11T09:23:18Zen
dc.identifier.urihttps://hdl.handle.net/10568/29363
dc.titleRegulation of the growth and differentiation of Trypanosoma (Trypanozoon) brucei brucei in resistant (C57B1/6) and susceptible (C3H/He) miceen
dcterms.abstractSummary While Trypanosoma brucei brucei GUTat 3 were equally infective for C3H/Heand for C57B1/6 mice at doses ranging from 5 to 5 × 103 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 103 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.en
dcterms.accessRightsLimited Access
dcterms.available2007-10-09
dcterms.bibliographicCitationParasite Immunology;5: 465-478en
dcterms.extentp. 465-478en
dcterms.issued1983-09
dcterms.languageen
dcterms.licenseCopyrighted; all rights reserved
dcterms.publisherWileyen
dcterms.subjecttrypanosoma bruceien
dcterms.subjectdisease resistanceen
dcterms.subjectmiceen
dcterms.subjectanimal diseasesen
dcterms.subjectimmunologyen
dcterms.subjectparasitologyen
dcterms.typeJournal Article

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