Clumping factor A of Staphylococcus aureus inhibits phagocytosis by human polymorphonuclear leucocytes
Clumping factor A of Staphylococcus aureus inhibits phagocytosis by human polymorphonuclear leucocytes
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DOI：
10.1111/j.1574-6968.2006.00229.x
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发表时间：
2006-05-01
影响因子：
2.1
通讯作者：
Foster, TJ
中科院分区：
文献类型：
--
作者：
Higgins, J;Loughman, A;Foster, TJ
金黄色葡萄球菌是医院和社区获得性感染的主要原因。它表达了几个促进多形核白细胞避免吞噬的因素。凝集因子A （ClfA）是金黄色葡萄球菌的一种纤维蛋白原结合表面蛋白，在多种感染模型中是重要的毒力因子。本研究探讨了ClfA是否是一种抗吞噬因子，以及其抗吞噬性能是否基于其结合纤维蛋白原的能力。在金黄色葡萄球菌中，ClfA被证明与蛋白A同等重要，后者的抗吞噬特性已经确立。在革兰氏阳性宿主中表达的ClfA也被发现具有抗吞噬作用。在缺乏纤维蛋白原的情况下，不能结合纤维蛋白原的ClfA突变体具有与天然ClfA相似的抗吞噬作用。在没有纤维蛋白原的情况下，ClfA抑制吞噬作用，在有纤维蛋白原的情况下，其抑制作用增强。
Staphylococcus aureus is a major cause of nosocomial and community-acquired infection. It expresses several factors that promote avoidance of phagocytosis by polymorphonuclear leucocytes. Clumping factor A (ClfA) is a fibrinogen-binding surface protein of S. aureus that is an important virulence factor in several infection models. This study investigated whether ClfA is an antiphagocytic factor, and whether its antiphagocytic properties were based on its ability to bind fibrinogen. In S. aureus, ClfA was shown to be of equal importance to protein A, the antiphagocytic properties of which are well established. ClfA expressed in a surrogate Gram-positive host was also found to be antiphagocytic. A ClfA mutant that was unable to bind fibrinogen had a similar antiphagocytic effect to native ClfA in the absence of fibrinogen. ClfA inhibited phagocytosis in the absence of fibrinogen, and showed enhanced inhibition in the presence of fibrinogen.