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首页> 外文期刊>Infection and immunity >Phagocytic Receptors Dictate Phagosomal Escape and Intracellular Proliferation of Francisella tularensis
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Phagocytic Receptors Dictate Phagosomal Escape and Intracellular Proliferation of Francisella tularensis

机译：吞噬细胞受体决定了土拉弗朗西斯菌的吞噬逃逸和细胞内增殖。

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Francisella tularensis, the causative agent of tularemia, survives and proliferates within macrophages of the infected host as part of its pathogenic strategy, through an intracellular life cycle that includes phagosomal escape and extensive proliferation within the macrophage cytosol. Various in vitro models of Francisella-macrophage interactions have been developed, using either opsonic or nonopsonic phagocytosis, and have generated discrepant results on the timing and extent of Francisella phagosomal escape. Here we have investigated whether either complement or antibody opsonization of the virulent prototypical type A strain Francisella tularensis subsp. tularensis Schu S4 affects its intracellular cycle within primary murine bone marrow-derived macrophages. Opsonization of Schu S4 with either human serum or purified IgG enhanced phagocytosis but restricted phagosomal escape and intracellular proliferation. Opsonization of Schu S4 with either fresh serum or purified antibodies redirected bacteria from the mannose receptor (MR) to the complement receptor CR3, the scavenger receptor A (SRA), and the Fcγ receptor (FcγR), respectively. CR3-mediated uptake delayed maturation of the early Francisella-containing phagosome (FCP) and restricted phagosomal escape, while FcγR-dependent phagocytosis was associated with superoxide production in the early FCP and restricted phagosomal escape and intracellular growth in an NADPH oxidase-dependent manner. Taken together, these results demonstrate that opsonophagocytic receptors alter the intracellular fate of Francisella by delivering bacteria through phagocytic pathways that restrict phagosomal escape and intracellular proliferation.
机译：tularemia的病原体Francisella tularensis通过被感染的宿主的巨噬细胞胞质内的吞噬逃逸和广泛增殖的细胞内生命周期，在感染宿主的巨噬细胞内生存和增殖。利用调理吞噬或非调理吞噬作用，已开发出各种弗朗西斯菌-巨噬细胞相互作用的体外模型，并在弗朗西斯菌吞噬体逃逸的时间和程度方面产生了不同的结果。在这里，我们研究了强毒原型A型弗朗西斯菌Tularensis亚种的补体或抗体调理作用。 tularensis Schu S4影响其在原代小鼠骨髓来源的巨噬细胞内的细胞内循环。人血清或纯化的IgG对Schu S4的调理作用可增强吞噬作用，但会限制吞噬体逃逸和细胞内增殖。用新鲜的血清或纯化的抗体对Schu S4进行调理，可将细菌从甘露糖受体（MR）分别重定向至补体受体CR3，清道夫受体A（SRA）和Fcγ受体（FcγR）。 CR3介导的摄取延迟了早期含弗朗西斯菌的吞噬体（FCP）的成熟并限制了吞噬体的逃逸，而FcγR依赖的吞噬作用与FCP早期的超氧化物产生和以NADPH氧化酶依赖的方式限制了吞噬体的逃逸和细胞内生长有关。综上所述，这些结果表明调理吞噬受体通过通过限制吞噬体逃逸和细胞内增殖的吞噬途径递送细菌来改变弗氏杆菌的细胞内命运。

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