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首页> 外文期刊>Infection and immunity >Acquired Resistance but Not Innate Resistance toMycobacterium bovis Bacillus Calmette-Guérin Is Compromised by Interleukin-12 Ablation
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Acquired Resistance but Not Innate Resistance toMycobacterium bovis Bacillus Calmette-Guérin Is Compromised by Interleukin-12 Ablation

机译：白介素12消融削弱了对牛分枝杆菌卡介苗的固有抗性，但不是先天抗性

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Interleukin-12 (IL-12) is one of the first cytokines produced by macrophages, key mediators of innate resistance, during the host’s immune response to infections. Therefore, in this study we propose that IL-12 has an important role in the early phase of the immune response to Mycobacterium bovis BCG. IL-12 has been shown to enhance the maturation of protective Th1 cells and gamma interferon (IFN-γ) production during mycobacterial infection. Therefore, it may play a crucial role during the immune phase of infection as well. To examine the role of IL-12 in both the innate and the immune phase of infection, we compared BCG-resistant mice, B10.A (Bcgr ), to the susceptible congenic strain B10.A (Bcgs ) following administration of a blocking monoclonal antibody to IL-12 (10F6). Anti-IL-12-treated susceptible animals exhibited a two- to threefold increase in spleen CFU by day 21. In contrast, anti-IL-12 treatment had little or no effect on the response of the genetically resistant animals to infection. The B10.A (Bcgr ) but not the B10.A (Bcgs ) mice had an increase in IFN-γ mRNA relative to baseline levels as early as day 1 of infection irrespective of anti-IL-12 treatment. By day 14, B10.A (Bcgr ) mice showed a decrease in IFN-γ mRNA while the B10.A (Bcgs ) mice showed a significant increase in IFN-γ mRNA levels. Thus, during BCG infection, the B10.A (Bcgr ) mice mount an early IFN-γ response against BCG whereas the B10.A (Bcgs ) mice have a delayed IFN-γ response correlating with their genetic permissiveness expressed as an increased mycobacterial load by day 21. Overall, our data demonstrate that the inherent resistance of B10.A (Bcgr ) mice to mycobacteria does not depend on optimal levels of IL-12 to maintain effective control of the bacteria, whereas IL-12 is important for the susceptible animals’ response to BCG during the peak of infection.
机译：白细胞介素12（IL-12）是宿主对感染的免疫反应过程中，巨噬细胞（先天性抗性的关键介体）产生的首批细胞因子之一。因此，在这项研究中，我们提出IL-12在对牛分枝杆菌BCG的免疫应答的早期阶段中起重要作用。 IL-12已显示在分枝杆菌感染过程中增强保护性Th1细胞的成熟和γ干扰素（IFN-γ）的产生。因此，它在感染的免疫阶段也可能起关键作用。为了检查IL-12在感染的自然阶段和免疫阶段中的作用，我们将抗BCG的小鼠B10.A（ Bcg r ）与给予IL-12（10F6）的封闭性单克隆抗体后，感染了B10.A（ Bcg s ）。抗IL-12处理的易感动物到第21天的脾脏CFU升高了2-3倍。相反，抗IL-12处理对遗传抗性动物对感染的反应几乎没有影响。 B10.A（ Bcg r ）而不是B10.A（ Bcg s ）小鼠增加与抗IL-12治疗无关，最早在感染第1天时，IFN-γmRNA相对于基线水平的水平就降低了。到第14天，B10.A（ Bcg r ）小鼠的IFN-γmRNA下降，而B10.A（ Bcg s ）小鼠的IFN-γmRNA水平显着增加。因此，在BCG感染期间，B10.A（ Bcg r ）小鼠对BCG产生了早期的IFN-γ反应，而B10.A（ Bcg > s ）小鼠的IFN-γ响应延迟，与它们的遗传容许性相关，到21天时分枝杆菌载量增加。总体而言，我们的数据表明B10.A（ Bcg r ）小鼠对分枝杆菌的依赖并不依赖于IL-12的最佳水平来维持对细菌的有效控制，而IL-12对于易感动物对BCG的反应很重要在感染高峰期。

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