单核细胞增生李斯特菌中CcpA缺失株的构建及对毒力的影响

CcpA是革兰氏阳性菌中由ccpA基因编码的介导碳分解代谢物阻遏的全局调控因子。近年来的研究表明，CcpA不仅参与CCR效应，还直接或间接参与病原细菌毒力基因的表达调控。为探讨CcpA对单核细胞增生李斯特菌（Lm）毒力的影响，应用同源重组方法构建CcpA缺失菌株。以BLAB/c小鼠为实验动物模型，检测野生株EGDe和缺失株EGDeΔccpA侵染小鼠后的半数致死剂量 LD₅₀和肝脾细菌载菌量，观察小鼠肝脏和脾脏的病理形态变化。结果显示：缺失CcpA后，Lm的LD₅₀降低了10倍，虽然肝脾细菌载菌量没有显著变化，但EGDe△ccpA对小鼠肝和脾的损害更为严重，表明CcpA缺失增强了细菌的毒力，CcpA 对Lm 毒力基因的表达可能具有间接或者直接的调控作用。

Effect of the Deletion of CcpA on Virulence in Listeria monocytogenes

CcpA, encoded by the ccpA gene, is the global mediator of carbon catabolite repression (CCR) in gram-positive bacteria. Increasing evidences suggest that CcpA not only participate in CCR, but also regulate the expression of virulence genes in pathogenic bacteria directly or indirectly. To investigate the effect of CcpA on virulence of Listeria monocytogenes, CcpA deletion strain was constructed using homologous recombination. The LD₅₀ of the wild strain EGDe and EGDeΔccpA for BLAB/c mice was measured, the amount of bacteria in liver and spleen was counted, and pathological changes of liver and spleen were observed. The results showed that compared to EGDe, the LD₅₀ of EGDeΔccpA reduced by 10 times, and lesion caused by EGDeΔccpA in liver and spleen of mice was more severe, indicating that deletion of CcpA enhances bacterial virulence in L. monocytogenes, CcpA might regulate L. monocytogenes, virulence gene expression directly or indirectly.