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The Streptococcus pneumoniae Capsule Inhibits Complement Activity and Neutrophil Phagocytosis by Multiple Mechanisms▿

机译：肺炎链球菌胶囊通过多种机制抑制补体活性和中性粒细胞吞噬

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The Streptococcus pneumoniae capsule is vital for virulence and may inhibit complement activity and phagocytosis. However, there are only limited data on the mechanisms by which the capsule affects complement and the consequences for S. pneumoniae interactions with phagocytes. Using unencapsulated serotype 2 and 4 S. pneumoniae mutants, we have confirmed that the capsule has several effects on complement activity. The capsule impaired bacterial opsonization with C3b/iC3b by both the alternative and classical complement pathways and also inhibited conversion of C3b bound to the bacterial surface to iC3b. There was increased binding of the classical pathway mediators immunoglobulin G (IgG) and C-reactive protein (CRP) to unencapsulated S. pneumoniae, indicating that the capsule could inhibit classical pathway complement activity by masking antibody recognition of subcapsular antigens, as well as by inhibiting CRP binding. Cleavage of serum IgG by the enzyme IdeS reduced C3b/iC3b deposition on all of the strains, but there were still marked increases in C3b/iC3b deposition on unencapsulated TIGR4 and D39 strains compared to encapsulated strains, suggesting that the capsule inhibits both IgG-mediated and IgG-independent complement activity against S. pneumoniae. Unencapsulated strains were more susceptible to neutrophil phagocytosis after incubation in normal serum, normal serum treated with IdeS, complement-deficient serum, and complement-deficient serum treated with IdeS or in buffer alone, suggesting that the capsule inhibits phagocytosis mediated by Fcγ receptors, complement receptors, and nonopsonic receptors. Overall, these data show that the S. pneumoniae capsule affects multiple aspects of complement- and neutrophil-mediated immunity, resulting in a profound inhibition of opsonophagocytosis.
机译：肺炎链球菌胶囊对毒力至关重要，并可能抑制补体活性和吞噬作用。然而，关于胶囊影响补体的机制以及肺炎链球菌与吞噬细胞相互作用的后果的数据尚有限。使用未封装的血清型2和4肺炎链球菌突变体，我们已经确认该胶囊对补体活性具有多种作用。胶囊通过替代途径和经典补体途径均损害了C3b / iC3b的细菌调理作用，并且还抑制了与细菌表面结合的C3b向iC3b的转化。经典途径介质免疫球蛋白G（IgG）和C反应蛋白（CRP）与未包囊的肺炎链球菌的结合增加，这表明该胶囊可通过掩盖抗体对包膜下抗原的识别以及抑制CRP结合。酶IdeS切割血清IgG减少了所有菌株上的C3b / iC3b沉积，但是与包囊菌株相比，未包囊的TIGR4和D39菌株上C3b / iC3b沉积仍显着增加，这表明该胶囊同时抑制了IgG介导的两种IgG和针对肺炎链球菌的IgG非依赖性补体活性。未封装的菌株在正常血清，经IdeS处理的正常血清，补体缺陷型血清和经IdeS处理的补体缺陷型血清或仅在缓冲液中孵育后，对中性粒细胞吞噬作用更敏感，这表明该胶囊可抑制Fcγ受体介导的吞噬作用受体和非声光受体。总的来说，这些数据表明肺炎链球菌胶囊影响补体和嗜中性粒细胞介导的免疫的多个方面，从而严重抑制调理吞噬作用。

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