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首页> 外文期刊>Infection and immunity >Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice
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Macrophages Are Critical for Cross-Protective Immunity Conferred by Babesia microti against Babesia rodhaini Infection in Mice

机译：巨噬细胞对于微量巴贝氏菌赋予小鼠抗罗氏杆菌的交叉保护免疫至关重要

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Although primary infection of mice with Babesia microti has been shown to protect mice against subsequent lethal infection by Babesia rodhaini, the mechanism behind the cross-protection is unknown. To unravel this mechanism, we investigated the influence of primary infection of mice with nonlethal B. microti using different time courses on the outcome of subsequent lethal B. rodhaini infection. Simultaneous infections of mice with these parasites resulted in rapid increases in parasitemia, with 100% mortality in BALB/c mice, as observed with control mice infected with B. rodhaini alone. In contrast, mice with acute, resolving, and chronic-phase B. microti infections were completely protected against B. rodhaini, resulting in low parasitemia and no mortalities. Mice immunized with dead B. microti were not protected from B. rodhaini infection, although high antibody responses were induced. Interestingly, the protected mice had significantly decreased levels of antibody response, cytokines (including gamma interferon [IFN-γ], interleukin-2 [IL-2], IL-8, IL-10, and IL-12), and nitric oxide levels after infection with B. rodhaini. SCID mice and IFN-γ-deficient mice with chronic B. microti infections demonstrated protective responses comparable to those of immunocompetent mice. Likewise, in vivo NK cell depletion did not significantly impair the protective responses. Conversely, macrophage depletion resulted in increased susceptibility to B. rodhaini infection associated with changes in their antibody and cytokines profiles, indicating that macrophages contribute to the protection against this challenge infection. We conclude that future development of vaccines against Babesia should include a strategy that enhances the appropriate activation of macrophages.
机译：尽管已经显示出用小巴贝氏菌引起的小鼠的初次感染可以保护小鼠免受随后的罗氏巴贝氏菌的致死性感染，但交叉保护的机制尚不清楚。为了阐明这种机制，我们调查了使用不同时间进程的非致死性小肠博德特氏菌对小鼠的初次感染对随后的致死性罗德氏梭状芽孢杆菌感染结果的影响。用这些寄生虫同时感染小鼠会导致寄生虫病迅速增加，在BALB / c小鼠中死亡率达到100％，与仅感染罗狄氏双歧杆菌的对照小鼠所观察到的一样。相比之下，患有急性，解决性和慢性期小肠双歧杆菌感染的小鼠可完全抵抗罗氏芽孢杆菌，从而导致低寄生虫血症且无死亡。尽管已诱导了高抗体反应，但死去的微小博德特氏菌免疫的小鼠并未受到罗德氏芽孢杆菌感染的保护。有趣的是，受保护的小鼠的抗体应答，细胞因子（包括γ干扰素[IFN-γ]，白介素-2 [IL-2]，IL-8，IL-10和IL-12）和一氧化氮水平显着降低。感染杆状芽孢杆菌后的水平。 SCID小鼠和慢性B. microti感染的IFN-γ缺陷小鼠表现出的保护性反应与具有免疫能力的小鼠相当。同样，体内NK细胞耗竭也没有明显损害保护反应。相反，巨噬细胞耗竭导致对罗伊氏芽孢杆菌感染的易感性增加，这与其抗体和细胞因子谱的变化有关，这表明巨噬细胞有助于抵抗这种挑战性感染。我们得出结论，针对巴贝虫病的疫苗的未来开发应包括增强巨噬细胞适当激活的策略。

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