González-Zorn B, Domínguez-Bernal G, Suárez M, Ripio M T, Vega Y, Novella S, Rodríguez A, Chico I, Tierrez A, Vázquez-Boland J A
Grupo de Patogénesis Molecular Bacteriana, Facultad de Veterinaria, Universidad Complutense de Madrid, Spain.
Int J Med Microbiol. 2000 Oct;290(4-5):369-74. doi: 10.1016/S1438-4221(00)80044-2.
We describe here the fourth listerial membrane-damaging virulence factor, a sphingomyelinase C (SMase) that is produced specifically by the ruminant pathogen Listeria ivanovii. Its coding gene, smcL, is a monocistron expressed independently of PrfA. The smcL product, SmcL, is highly similar to the staphylococcal beta-toxin and is responsible for the differential hemolytic properties of L. ivanovii (bizonal hemolysis and CAMP-like reaction with R. equi). The role of SmcL in virulence was assessed by gene disruption and complementation. Our data show that SmcL mediates disruption of the membrane of primary phagosomes, thereby promoting bacterial intracellular proliferation. They also suggest that SmcL may play a role in host tropism. smcL is located in LIPI-2, a novel 18-kb pathogenicity island which also contains a cluster of internalin genes. LIPI-2 is unstable, L. ivanovii-specific and required for full virulence in mice and lambs.
我们在此描述了李斯特菌的第四个膜损伤毒力因子，一种由反刍动物病原菌伊氏李斯特菌特异性产生的鞘磷脂酶C（SMase）。其编码基因smcL是一个独立于PrfA表达的单顺反子。smcL产物SmcL与葡萄球菌β毒素高度相似，并导致伊氏李斯特菌具有不同的溶血特性（双区溶血以及与马红球菌的CAMP样反应）。通过基因敲除和互补实验评估了SmcL在毒力中的作用。我们的数据表明，SmcL介导初级吞噬体膜的破坏，从而促进细菌在细胞内的增殖。数据还表明，SmcL可能在宿主嗜性方面发挥作用。smcL位于LIPI-2中，LIPI-2是一个新的18 kb致病岛，其中还包含一组内化素基因。LIPI-2不稳定，具有伊氏李斯特菌特异性，是小鼠和羔羊完全毒力所必需的。
