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首页> 外文期刊>Infection and immunity >Role of Complement in Mycobacterium avium Pathogenesis: In Vivo and In Vitro Analyses of the Host Response to Infection in the Absence of Complement Component C3
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Role of Complement in Mycobacterium avium Pathogenesis: In Vivo and In Vitro Analyses of the Host Response to Infection in the Absence of Complement Component C3

机译：补体在鸟分枝杆菌发病机理中的作用：在缺乏补体成分C3的情况下对宿主对感染的反应的体内和体外分析

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We investigated the importance of the host complement system in the pathogenesis of disease mediated by the intramacrophage pathogenMycobacterium avium. Mycobacteria opsonized with complement are efficiently ingested by macrophages through various complement receptors. Furthermore, unlike other bacteria, mycobacteria can activate both the alternative and classical complement pathways in the absence of specific antibodies. Therefore, to examine the role of complement in the mycobacterial infection process in vivo, mice deficient in complement component C3 were infected with M. avium. Surprisingly, C3-deficient mice infected intravenously with M. avium displayed no difference in bacterial burden or granulomatous response compared to wild-type control mice. C3-sufficient mice and C3-deficient mice were equally susceptible to infection by M. avium regardless of the genotype at thebcg locus, a locus known to confer susceptibility to infection with intracellular pathogens. In vitro studies using mouse bone marrow-derived macrophages resulted in significant M. avium invasion of macrophages in the absence of C3; however, the kinetics of infection were delayed compared to complement-mediated invasion. The data indicate that complement does not play an essential role in mediating M. avium infections in the mouse and suggest either that other invasion mechanisms can compensate for the absence of complement-mediated entry or that complement is not a major mycobacterial opsonin in vivo.
机译：我们研究了宿主补体系统在巨噬细胞内病原体鸟分枝杆菌介导的疾病发病机理中的重要性。被补体调理的分枝杆菌被巨噬细胞通过各种补体受体有效地摄取。此外，与其他细菌不同，分枝杆菌可以在不存在特异性抗体的情况下激活替代途径和经典补体途径。因此，为了检查补体在体内分枝杆菌感染过程中的作用，将补体成分C3缺陷的小鼠感染了 M。 令人惊讶的是，C3缺陷型小鼠静脉感染了 M。 avium 与野生型对照小鼠相比，细菌负荷或肉芽肿反应无差异。 C3充足的小鼠和C3不足的小鼠同样易受M感染。 avium ，而与 bcg 位点的基因型无关，该位点已知会引起细胞内病原体感染的易感性。使用小鼠骨髓来源的巨噬细胞进行的体外研究导致明显的M。在没有C3的情况下巨噬细胞的鸟卵入侵;然而，与补体介导的侵袭相比，感染的动力学被延迟了。数据表明补体在介导 M中没有起重要作用。小鼠感染鸟卵并表明其他入侵机制可以弥补补体介导的进入的缺乏，或者补体不是体内主要的分枝杆菌调理素。

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