Josefsson E, Hartford O, O'Brien L, Patti J M, Foster T
Department of Rheumatology, University of Göteborg, Göteborg, Sweden.
J Infect Dis. 2001 Dec 15;184(12):1572-80. doi: 10.1086/324430. Epub 2001 Dec 3.
The importance of the fibrinogen-binding adhesin clumping factor A (ClfA) in the pathogenesis of Staphylococcus aureus septic arthritis was examined in an animal model. The protective effect of active and passive immunization with ClfA also was investigated in S. aureus infection models. The severity of arthritis was markedly reduced in mice challenged intravenously with a clfA mutant, compared with mice infected with the wild-type strain. Mice immunized with recombinant ClfA and challenged with S. aureus developed less-severe arthritis than did mice immunized with a control antigen. Passive immunization of mice with rat and rabbit anti-ClfA antibodies protected against S. aureus arthritis and sepsis-induced death, indicating that the protection by active immunization is antibody mediated. Taken together, these data strongly suggest that ClfA is a crucial virulence determinant for septic arthritis and an excellent target for the generation of immune therapies directed against S. aureus.
在动物模型中研究了纤维蛋白原结合黏附素聚集因子A（ClfA）在金黄色葡萄球菌败血症性关节炎发病机制中的重要性。还在金黄色葡萄球菌感染模型中研究了用ClfA进行主动和被动免疫的保护作用。与感染野生型菌株的小鼠相比，用clfA突变体静脉内攻击的小鼠关节炎严重程度明显降低。用重组ClfA免疫并用金黄色葡萄球菌攻击的小鼠比用对照抗原免疫的小鼠发生的关节炎症状较轻。用大鼠和兔抗ClfA抗体对小鼠进行被动免疫可预防金黄色葡萄球菌性关节炎和败血症诱导的死亡，表明主动免疫的保护作用是由抗体介导的。综上所述，这些数据强烈表明ClfA是败血症性关节炎的关键毒力决定因素，也是针对金黄色葡萄球菌的免疫疗法的理想靶点。
