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首页> 外文OA文献 >Use of an Attenuated Leishmanial Parasite as an Immunoprophylactic and Immunotherapeutic Agent against Murine Visceral Leishmaniasis
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Use of an Attenuated Leishmanial Parasite as an Immunoprophylactic and Immunotherapeutic Agent against Murine Visceral Leishmaniasis

机译：减毒的利什曼原虫作为抗小鼠内脏利什曼病的免疫预防和免疫治疗剂的用途

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The ability of the leishmanial parasite UR6 to act as an immunoprophylactic and immunotherapeutic agent against Leishmania donovani infection in BALB/c mice was investigated. Unlike the virulent L. donovani AG83 (MOHOM/IN/1983/AG83), UR6 given through intracardiac route failed to induce visceral infection, but when it was injected subcutaneously, UR6 induced a short-lived and localized self-healing skin lesion. Priming of peritoneal macrophages with UR6 in vitro induced superoxide (O2−) generation, whereas similar experiments with virulent AG83 inhibited O2− generation. It was observed that priming of mice with either live or sonicated UR6 in the absence of any adjuvant provided strong protection against subsequent virulent challenge. Further, UR6-primed infected mice not only displayed a strong antileishmanial delayed-type hypersensitivity (DTH) response but also showed an elevated level of the serum antileishmanial immunoglobulin G2a (IgG2a) isotype, whereas infected mice failed to mount any antileishmanial DTH response and showed an elevated level of IgG1. This indicates that UR6 priming and subsequent L. donovani infection allowed the expansion of Th1 cells. Our studies indicate that UR6 has potential to be used as an immunoprophylactic and immunotherapeutic agent against experimental visceral leishmaniasis.
机译：研究了利什曼原虫UR6充当针对BALB / c小鼠中的利什曼原虫donovani感染的免疫预防剂和免疫治疗剂的能力。与强毒的多诺尼乳杆菌AG83（MOHOM / IN / 1983 / AG83）不同，通过心内途径给予的UR6不能诱导内脏感染，但是当皮下注射时，UR6会引起短暂且局部的自我修复的皮肤病变。在体外用UR6引发腹膜巨噬细胞引发了超氧化物（O2-）的生成，而类似的用有毒力的AG83进行的实验则抑制了O2-的生成。观察到，在没有任何佐剂的情况下，用活的或超声处理的UR6引发的小鼠对随后的强毒攻击提供了强大的保护。此外，UR6引发的感染小鼠不仅表现出强烈的抗血管紧张素延迟型超敏反应（DTH），而且还显示血清抗血管紧张素原免疫球蛋白G2a（IgG2a）同种型水平升高，而受感染的小鼠未能引起任何抗血管紧张素DTH反应并显示出IgG1水平升高。这表明UR6引发和随后的多诺氏乳杆菌感染允许Th1细胞扩增。我们的研究表明，UR6有潜力用作针对实验性内脏利什曼病的免疫预防和免疫治疗剂。

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