کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3394406 1221463 2008 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Influence of Brugia malayi life stages and BmAFII fraction on experimental Leishmania donovani infection in hamsters
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی انگل شناسی
پیش نمایش صفحه اول مقاله
Influence of Brugia malayi life stages and BmAFII fraction on experimental Leishmania donovani infection in hamsters
چکیده انگلیسی

The influence of live Brugia malayi parasites and a Sephadex G-200 fraction of the adult parasite extract (BmAFII) on the progression of Leishmania donovani infection was studied. Inbred hamsters were first infected with B. malayi infective 3rd stage larvae (L3), adult worms or microfilariae (mf), and then with L. donovani amastigotes (Ld), or vice versa or received both the infections simultaneously; a group of animals were first immunized with BmAFII and then infected with Ld. L. donovani parasite burden was determined between 17 and 19 days post amastigote challenge (p.a.c.) and, in case of immunized animals, between 32 and 35 days p.a.c also. Nitric oxide (NO) release from peritoneal macrophages and cellular proliferative responses of lymphnode cells were assessed in BmAFII-immunized animals given leishmania infection or no infection. Leishmanial parasite burden was significantly reduced in animals exposed to filarial L3 before amastigote inoculation and in animals given filarial adult worms after or together with amastigotes. Prior immunization of leishmania-infected animals with BmAFII also reduced the leishmanial parasite burden (17–19 days p.a.c.: >90%; 32–35 days p.a.c.: 60%). These animals showed upregulation of NO release and cellular proliferative responses to promastigote antigen or BmAFII stimulation in vitro. The findings show, for the first time, that B. malayi L3/adult worms or immunization with BmAFII inhibits progression of L. donovani infection in hamsters and this is associated with upregulation of NO and lymphocyte proliferative responses indicating that Th1 response might be responsible for this.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Acta Tropica - Volume 106, Issue 2, May 2008, Pages 81–89
نویسندگان
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