Lowrance J H, Baddour L M, Simpson W A
H.S. Truman Veterans Administration Hospital, University of Missouri, Columbia 65201.
J Clin Invest. 1990 Jul;86(1):7-13. doi: 10.1172/JCI114717.
Inactivation of fibronectin (Fn) binding by insertional mutagenesis of Streptococcus sanguis with Tn916 reduces virulence of this bacterium in the rat model of infective endocarditis (IE). Transconjugants were screened for Fn adherence using an ELISA adherence test. One transconjugant had a decreased adherence to immobilized Fn. Southern hybridization demonstrated that the insertion occurred only once in this mutant. The parent strain and mutant strain JL113 were used as challenge strains in a rat endocarditis model. These experiments demonstrated that the mutant had a reduced ability (P less than 0.05) to produce IE. Spontaneous excision of Tn916 from JL113 produced strains identical to both the parental and mutant phenotypes. One strain (JLR-19) that retained the mutant phenotype and one (JLR-15) that regained the parental phenotype for Fn binding were tested for their ability to produce IE. These strains demonstrated that the ability to bind Fn and to produce IE were correlated after Tn916 excision. The reduced virulence of the mutant suggested that adherence of S. sanguis to immobilized Fn plays an important role in the production of IE.
用Tn916对血链球菌进行插入诱变使纤连蛋白（Fn）结合失活，降低了该细菌在感染性心内膜炎（IE）大鼠模型中的毒力。使用ELISA粘附试验筛选转接合子的Fn粘附情况。一个转接合子对固定化Fn的粘附减少。Southern杂交表明该突变体中仅发生了一次插入。亲本菌株和突变菌株JL113用作大鼠心内膜炎模型的攻击菌株。这些实验表明，该突变体产生IE的能力降低（P小于0.05）。Tn916从JL113中自发切除产生的菌株与亲本和突变体表型均相同。测试了一株保留突变体表型的菌株（JLR-19）和一株恢复亲本Fn结合表型的菌株（JLR-15）产生IE的能力。这些菌株表明，Tn916切除后，Fn结合能力与产生IE的能力相关。突变体毒力降低表明血链球菌对固定化Fn的粘附在IE产生中起重要作用。
