Schennings T, Heimdahl A, Coster K, Flock J I
Center for Biotechnology, Karolinska Institute, Huddinge, Sweden.
Microb Pathog. 1993 Sep;15(3):227-36. doi: 10.1006/mpat.1993.1073.
Rats were immunized with a fusion protein (gal-FnBP) encompassing beta-galactosidase and the domains of fibronectin binding protein from Staphylococcus aureus responsible for binding to fibronectin. Antibodies against gal-FnBP were shown to block the binding of S. aureus to immobilized fibronectin in vitro. Endocarditis in immunized and non-immunized control rats was induced by catheterization via the right carotid artery, resulting in damaged aortic heart valves which became covered by fibrinogen and fibronectin. The catheterized rats were then infected intravenously with 1 x 10(5) cells of S. aureus. The number of bacteria associated with aortic valves was determined 1 1/2 days after the challenge infection and a significant difference in bacterial numbers between immunized and non-immunized groups was then observed (p < 0.05).
用一种融合蛋白(gal-FnBP)对大鼠进行免疫,该融合蛋白包含β-半乳糖苷酶和金黄色葡萄球菌中负责与纤连蛋白结合的纤连蛋白结合蛋白结构域。已证明抗gal-FnBP抗体在体外可阻断金黄色葡萄球菌与固定化纤连蛋白的结合。通过右颈动脉插管在免疫和未免疫的对照大鼠中诱发心内膜炎,导致主动脉心脏瓣膜受损,瓣膜上覆盖有纤维蛋白原和纤连蛋白。然后通过静脉注射1×10⁵个金黄色葡萄球菌细胞对插管大鼠进行感染。在攻击感染后1.5天测定与主动脉瓣膜相关的细菌数量,随后观察到免疫组和未免疫组之间的细菌数量存在显著差异(p<0.05)。