Inhibition of complement activation by a secreted Staphylococcus aureus protein
Inhibition of complement activation by a secreted Staphylococcus aureus protein
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DOI：
10.1086/422259
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发表时间：
2004-08-01
影响因子：
6.4
通讯作者：
Brown, EL
中科院分区：
文献类型：
--
作者：
Lee, LYL;Höök, M;Brown, EL
金黄色葡萄球菌可引起多种急、慢性疾病。S.金黄色葡萄球菌引起持续性感染与其逃避或逃避宿主免疫反应的能力有关。我们已经确定了一个分泌的19 kDa的蛋白产生的S。金黄色葡萄球菌结合补体蛋白C3。该蛋白的N-末端测序鉴定其为细胞外纤维蛋白原结合蛋白（Efb）。在这项研究中，我们证明Efb可以结合到C3的α链，并抑制补体激活的经典和替代途径。此外，我们表明，EFB可以抑制补体介导的调理吞噬作用的剂量依赖性的方式和EFB抑制补体活性通过阻断沉积的C3或通过防止进一步的补体激活超过C3 b。这些数据表明，Efb是一个毒力因子参与促进持久的S。金黄色葡萄球菌感染通过干扰体内补体活性。
Staphylococcus aureus can cause a variety of acute and chronic diseases. The ability of S. aureus to cause persistent infections has been linked to its ability to evade or inactivate host immune responses. We have identified a secreted 19-kDa protein produced by S. aureus that binds to the complement protein C3. N-terminal sequencing of this protein identified it as the extracellular fibrinogen-binding protein (Efb). In this study, we demonstrate that Efb can bind to the alpha-chain of C3 and inhibit both the classical and alternative pathways of complement activation. In addition, we show that Efb can inhibit complement-mediated opsonophagocytosis in a dose-dependent manner and that Efb inhibits complement activity by blocking deposition of C3 or by preventing further complement activation beyond C3b. These data suggest that Efb is a virulence factor involved in facilitating persistent S. aureus infections by interfering with complement activity in vivo.