肺炎球菌表面蛋白C导致小鼠感染肺炎链球菌引起的败血症。
Pneumococcal surface protein C contributes to sepsis caused by Streptococcus pneumoniae in mice.
作者信息
Iannelli Francesco, Chiavolini Damiana, Ricci Susanna, Oggioni Marco Rinaldo, Pozzi Gianni
机构信息
Department of Molecular Biology, University of Siena, 53100 Siena, Italy.
出版信息
Infect Immun. 2004 May;72(5):3077-80. doi: 10.1128/IAI.72.5.3077-3080.2004.
Abstract
The role of pneumococcal surface protein C (PspC; also called SpsA, CbpA, and Hic) in sepsis by Streptococcus pneumoniae was investigated in a murine infection model. The pspC gene was deleted in strains D39 (type 2) and A66 (type 3), and the mutants were tested by being injected intravenously into mice. The animals infected with the mutant strains showed a significant increase in survival, with the 50% lethal dose up to 250-fold higher than that for the wild type. Our findings indicate that PspC affords a decisive contribution to sepsis development.
摘要
在小鼠感染模型中研究了肺炎链球菌表面蛋白C（PspC；也称为SpsA、CbpA和Hic）在肺炎链球菌败血症中的作用。在D39（2型）和A66（3型）菌株中删除了pspC基因，并通过静脉注射到小鼠体内对突变体进行测试。感染突变菌株的动物存活率显著提高，半数致死剂量比野生型高250倍。我们的研究结果表明，PspC对败血症的发展起决定性作用。
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