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Bacillus anthracis Phospholipases C Facilitate Macrophage-Associated Growth and Contribute to Virulence in a Murine Model of Inhalation Anthrax

机译:炭疽芽胞杆菌磷脂酶C促进巨噬细胞相关的生长,并在吸入性炭疽的鼠模型中促进毒力。

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Several models of anthrax pathogenesis suggest that early in the infectious process Bacillus anthracis endospores germinate and outgrow into vegetative bacilli within phagocytes before being released into the blood. Here, we define the respective contributions of three phospholipases C (PLCs) to the pathogenesis of B. anthracis. Genetic deletions of the PLCs were made in the Sterne 7702 background, resulting in the respective loss of their activities. The PLCs were redundant both in tissue culture and in murine models of anthrax. Deletion of all three PLC genes was required for attenuation of virulence in mice after intratracheal inoculation. This attenuation may be attributed to the inability of the PLC-null strain to grow in association with the macrophage. Complementation of these defects in both models of anthrax was achieved by expression of the PLC genes in trans. The functional redundancy between PLCs in the virulence of B. anthracis implies that their activities are important for anthrax pathogenesis.
机译:几种炭疽的发病机理模型表明,在感染过程中,炭疽杆菌的内生孢子在吞噬细胞内萌发并长出无性杆菌,然后释放到血液中。在这里,我们定义了三种磷脂酶C(PLC)对B的发病机理的各自贡献。炭疽。 PLC的遗传删除是在Sterne 7702背景中进行的,从而导致其各自的活动丧失。 PLC在组织培养和炭疽鼠模型中都是多余的。气管内接种后,为了减弱小鼠的毒性,需要删除所有三个PLC基因。该衰减可以归因于PLC无效株不能与巨噬细胞结合生长。通过在 trans 中表达PLC基因,实现了两种炭疽模型中这些缺陷的互补。 PLC在 B毒力下的功能冗余。炭疽表明它们的活性对于炭疽病的发病机理很重要。

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