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首页> 外文期刊>Infection and immunity >Escherichia coli msbB Gene as a Virulence Factor and a Therapeutic Target
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Escherichia coli msbB Gene as a Virulence Factor and a Therapeutic Target

机译：大肠杆菌msbB基因作为致病因子和治疗靶标

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A mutation in the msbB gene of Escherichia coli results in the synthesis of E. colilipopolysaccharide (LPS) that lacks the myristic acid moiety of lipid A. Although such mutant E. coli cells and their purified LPS have a greatly reduced ability to stimulate human immune cells, a minor reduction in the mouse inflammatory response is observed. When the msbB mutation is transferred into a clinical isolate ofE. coli, there is a significant loss in virulence, as assessed by lethality in BALB/c mice. When a cloned msbBgene is provided to functionally complement the msbBmutant, virulence returns, providing direct evidence that themsbB gene product is an important virulence factor in a murine model of E. coli pathogenicity. In the genetic background of the clinical E. coli isolate, themsbB mutation also results in filamentation of the cells at 37°C but not at 30°C, a reduction in the level of the K1 capsule, an increase in the level of complement C3 deposition, and an increase in both opsonic and nonopsonic phagocytosis of the msbBmutant, phenotypes that can help to explain the loss in virulence. The demonstration that the inhibition of msbB gene function reduces the virulence of E. coli in a mouse infection model warrants further investigation of the msbB gene product as a novel target for antibiotic therapy.
机译：大肠杆菌 msbB 基因的突变导致 E的合成。缺乏脂质A的肉豆蔻酸部分的大肠杆菌脂多糖（LPS）。大肠杆菌细胞及其纯化的LPS刺激人免疫细胞的能力大大降低，观察到小鼠炎症反应的轻微降低。当 msbB 突变转移到 E的临床分离株中时。大肠杆菌，通过致命性评估，BALB / c小鼠的毒力显着降低。当提供一个克隆的 msbB 基因以功能互补 msbB 突变体时，毒力会返回，这直接证明 msbB 基因产物是一种重要的毒力。 E鼠模型中的因子。致病性。在临床 E的遗传背景中。大肠杆菌分离株， msbB 突变也会导致细胞在37°C而不是30°C发生丝化，从而降低了K1胶囊的水平，并增加了水平补体C3沉积的变化，以及 msbB 突变体的调理吞噬和非调理吞噬作用的增加，可以帮助解释毒力的丧失。证明 msbB 基因功能的抑制会降低 E的毒力。小鼠感染模型中的大肠杆菌值得进一步研究 msbB 基因产物作为抗生素治疗的新靶标。

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