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首页> 外文期刊>Infection and immunity >Discriminating Virulence Mechanisms among Bacillus anthracis Strains by Using a Murine Subcutaneous Infection Model
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Discriminating Virulence Mechanisms among Bacillus anthracis Strains by Using a Murine Subcutaneous Infection Model

机译：用小鼠皮下感染模型鉴别炭疽芽孢杆菌菌株间的毒力机制

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Bacillus anthracis strains harboring virulence plasmid pXO1 that encodes the toxin protein protective antigen (PA), lethal factor, and edema factor and virulence plasmid pXO2 that encodes capsule biosynthetic enzymes exhibit different levels of virulence in certain animal models. In the murine model of pulmonary infection, B. anthracis virulence was capsule dependent but toxin independent. We examined the role of toxins in subcutaneous (s.c.) infections using two different genetically complete (pXO1+ pXO2+) strains of B. anthracis, strains Ames and UT500. Similar to findings for the pulmonary model, toxin was not required for infection by the Ames strain, because the 50% lethal dose (LD50) of a PA-deficient (PA?) Ames mutant was identical to that of the parent Ames strain. However, PA was required for efficient s.c. infection by the UT500 strain, because the s.c. LD50 of a UT500 PA? mutant was 10,000-fold higher than the LD50 of the parent UT500 strain. This difference between the Ames strain and the UT500 strain could not be attributed to differences in spore coat properties or the rate of germination, because s.c. inoculation with the capsulated bacillus forms also required toxin synthesis by the UT500 strain to cause lethal infection. The toxin-dependent phenotype of the UT500 strain was host phagocyte dependent, because eliminating Gr-1+ phagocytes restored virulence to the UT500 PA? mutant. These experiments demonstrate that the dominant virulence factors used to establish infection by B. anthracis depend on the route of inoculation and the bacterial strain.
机译：带有编码毒素蛋白保护性抗原（PA），致死因子和浮肿因子的毒力质粒pXO1的炭疽芽孢杆菌菌株和编码胶囊生物合成酶的毒力质粒pXO2在某些动物模型中显示出不同的毒力水平。在小鼠肺部感染模型中， B。炭疽病的毒力依赖于胶囊，但不依赖毒素。我们使用两种不同的 B遗传完全（pXO1 + pXO2 + ）菌株检查了毒素在皮下感染的作用。炭疽菌，菌株Ames和UT500。与肺部模型的发现相似，Ames菌株不需要感染毒素，因为50％致命剂量（LD 50 ）的PA缺乏（PA ？）Ames突变体与亲本Ames菌株相同。但是，PA是有效的s.c。由于s.c. UT500 PA ？突变体的LD 50 比亲本UT500菌株的LD 50 高10,000倍。 Ames菌株和UT500菌株之间的这种差异不能归因于孢子皮层性质或发芽率的差异，因为用荚膜芽孢杆菌形式接种也需要UT500菌株合成毒素以引起致命感染。 UT500菌株的毒素依赖性表型是宿主吞噬细胞依赖性的，因为消除Gr-1 + 吞噬细胞可恢复UT500 PA ？突变体的毒力。这些实验表明，主要的毒力因子用于确定B感染。炭疽病取决于接种途径和细菌菌株。

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