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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Genetic background affects the expansion of macrophage subsets in the lungs of Mycobacterium tuberculosis-infected hosts
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Genetic background affects the expansion of macrophage subsets in the lungs of Mycobacterium tuberculosis-infected hosts

机译：遗传背景影响结核分枝杆菌感染宿主肺中巨噬细胞亚群的扩增

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摘要

M1 macrophages are more effective in the induction of the inflammatory response and clearance of Mycobacterium tuberculosis than M2 macrophages. Infected C57BL/6 mice generate a stronger cellular immune response compared with BALB/c mice. We hypothesized that infected C57BL/6 mice would exhibit a higher frequency and function of M1 macrophages than infected BALB/c mice. Our findings show a higher ratio of macrophages to M2 macrophages in the lungs of chronically infected C57BL/6 mice compared with BALB/c mice. However, there was no difference in the functional ability of M1 and M2 macrophages for the two strains in vitro. In vivo, a deleterious role for M2 macrophages was confirmed by M2 cell transfer, which rendered the infected C57BL/6, but not the BALB/c mice, more susceptible and resulted in mild lung inflammation compared with C57BL/6 mice that did not undergo cell transfer. M1 cell transfer induced a higher inflammatory response, although not protective, in infected BALB/c mice compared with their counterparts that did not undergo cell transfer. These findings demonstrate that an inflammation mediated by M1 macrophages may not induce bacterial tolerance because protection depends on the host genetic background, which drives the magnitude of the inflammatory response against M. tuberculosis in the pulmonary microenvironment. The contribution of our findings is that although M1 macrophage is an effector leucocyte with microbicidal machinery, its dominant role depends on the balance of M1 and M2 subsets, which is driven by the host genetic background.
机译：M1巨噬细胞比M2巨噬细胞更有效地诱导炎症反应和结核分枝杆菌的清除。与BALB / c小鼠相比，感染的C57BL / 6小鼠产生更强的细胞免疫应答。我们假设感染的C57BL / 6小鼠比感染的BALB / c小鼠表现出更高的M1巨噬细胞频率和功能。我们的发现表明，与BALB / c小鼠相比，慢性感染的C57BL / 6小鼠肺中巨噬细胞与M2巨噬细胞的比例更高。但是，M1和M2巨噬细胞对两种菌株的体外功能能力没有差异。在体内，通过M2细胞转移证实了M2巨噬细胞的有害作用，与未接受感染的C57BL / 6小鼠相比，感染的C57BL / 6（而非BALB / c小鼠）更易感染并导致轻度肺部炎症细胞转移。与未进行细胞转移的小鼠相比，M1细胞转移在感染的BALB / c小鼠中诱导了更高的炎症反应，尽管不是保护性的。这些发现表明，由M1巨噬细胞介导的炎症可能不会诱导细菌耐受，因为保护取决于宿主的遗传背景，从而驱动了肺微环境中针对结核分枝杆菌的炎症反应。我们的发现的贡献在于，尽管M1巨噬细胞是具有杀微生物机制的效应白细胞，但其主导作用取决于宿主遗传背景所驱动的M1和M2亚群的平衡。

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