Ramos-Morales Francisco, Prieto Ana I, Beuzón Carmen R, Holden David W, Casadesús Josep
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Seville 41080, Spain.
J Bacteriol. 2003 Sep;185(17):5328-32. doi: 10.1128/JB.185.17.5328-5332.2003.
Passage through the digestive tract exposes Salmonella enterica to high concentrations of bile salts, powerful detergents that disrupt biological membranes. Mutations in the wecD or wecA gene, both of which are involved in the synthesis of enterobacterial common antigen (ECA), render S. enterica serovar Typhimurium sensitive to the bile salt deoxycholate. Competitive infectivity analysis of wecD and wecA mutants in the mouse model indicates that ECA is an important virulence factor for oral infection. In contrast, lack of ECA causes only a slight decrease in Salmonella virulence during intraperitoneal infection. A tentative interpretation is that ECA may contribute to Salmonella virulence by protecting the pathogen from bile salts.
通过消化道会使肠炎沙门氏菌暴露于高浓度的胆汁盐中,胆汁盐是破坏生物膜的强效去污剂。参与肠杆菌共同抗原(ECA)合成的wecD或wecA基因发生突变,会使鼠伤寒沙门氏菌血清型鼠伤寒杆菌对胆汁盐脱氧胆酸盐敏感。在小鼠模型中对wecD和wecA突变体进行的竞争性感染性分析表明,ECA是口腔感染的重要毒力因子。相比之下,缺乏ECA在腹腔感染期间仅使沙门氏菌毒力略有下降。一种初步解释是,ECA可能通过保护病原体免受胆汁盐的影响而有助于沙门氏菌的毒力。