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首页> 外文期刊>Infection and immunity >Effects of PspA and Antibodies to PspA on Activation and Deposition of Complement on the Pneumococcal Surface
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Effects of PspA and Antibodies to PspA on Activation and Deposition of Complement on the Pneumococcal Surface

机译：PspA和PspA抗体对肺炎球菌表面补体激活和沉积的影响

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Streptococcus pneumoniae infection is a frequent cause of pneumonia, otitis media, meningitis, and septicemia. Pneumococcal surface protein A (PspA) is an important virulence factor on the pathogen surface, and it is known to interfere with complement activation. In this study, flow cytometry was used to study the effects of PspA and antibodies to PspA on the deposition of complement C3 on the surface of a capsular type 3 strain, WU2, and its PspA? mutant, JY1119. Using naive mouse serum as a complement source, measurable deposition of C3 was observed within 4 min on PspA? pneumococci, and the amount of surface-bound C3 accumulated rapidly as the amount of serum was increased. In contrast, very little C3 was deposited on the PspA+ strain. In nonimmune mouse serum, the classical pathway was the dominant activation pathway triggered by PspA? pneumococci. Accordingly, EGTA blocked almost all of the complement activation. Moreover, a significant amount of C3 was still deposited on the PspA? strain when serum from factor B-deficient mice was used. This deposition was not observed on the PspA+ pneumococci, indicating that PspA may inhibit complement deposition via the classical pathway. Furthermore, under the conditions we tested, PspA also inhibited C3 deposition when the classical pathway was initiated by antibodies to capsular polysaccharide. Antibodies to PspA could overcome the anticomplementary effect of PspA, allowing for increased complement activation and C3 deposition onto PspA+ bacteria.
机译：肺炎链球菌感染是引起肺炎，中耳炎，脑膜炎和败血病的常见原因。肺炎球菌表面蛋白A（PspA）是病原体表面上的重要毒力因子，已知会干扰补体激活。本研究使用流式细胞仪研究PspA和抗PspA抗体对3型荚膜荚膜菌株WU2及其PspA ？突变体JY1119表面上补体C3沉积的影响。 。使用天然小鼠血清作为补体来源，可在4分钟内在PspA ？肺炎链球菌上观察到可测量的C3沉积，并且随着血清数量的增加，表面结合的C3的数量迅速积累。相反，几乎没有C3沉积在PspA + 菌株上。在非免疫小鼠血清中，经典途径是由肺炎链球菌PspA ？触发的显性激活途径。因此，EGTA阻断了几乎所有的补体激活。此外，当使用来自缺乏因子B的小鼠的血清时，大量的C3仍然沉积在PspA β菌株上。在PspA + 肺炎球菌上未观察到这种沉积，表明PspA可能通过经典途径抑制补体沉积。此外，在我们测试的条件下，当经典途径由荚膜多糖抗体引发时，PspA也抑制了C3沉积。 PspA抗体可以克服PspA的抗互补作用，从而增加补体激活和C3在PspA + 细菌上的沉积。

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