Su Jing, Timbely Dommo, Zhu Minmin, Hua Xiaomei, Liu Biao, Pang Yanjun, Shen Hengguan, Qi Jinliang, Yang Yonghua
State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Institute of Virology, Nanjing University, Nanjing, People's Republic of China.
Med Microbiol Immunol. 2009 Aug;198(3):185-94. doi: 10.1007/s00430-009-0115-8. Epub 2009 Apr 29.
In this study, a deletion mutant of rfaB (DeltarfaB) was observed to be susceptible to sodium dodecyl sulfate and less tolerant to bile salts. In addition, pre-incubation in 10% bile salts increased bacterial tolerance to 30% bile salts. We also showed that the DeltarfaB mutant invaded HeLa cells less than the wild type and resulted in a lower ratio of intracellular bacteria. Competitive infection of mice showed that the DeltarfaB mutant was defective in the colonization of host organs and was cleared more quickly in fecal shedding. Transforming of a plasmid containing a wild-type allele of rfaB (pRB3-rfaB) partially rescued the defect of the DeltarfaB mutant. The results suggest that RfaB, which is responsible to add the glycosyl residue to the core lipopolysaccharide, contributes to the tolerance to detergent and the virulence of Salmonella enterica serovar Enteritidis.
在本研究中，观察到rfaB的缺失突变体（DeltarfaB）对十二烷基硫酸钠敏感，对胆盐的耐受性较低。此外，在10%胆盐中预孵育可提高细菌对30%胆盐的耐受性。我们还表明，DeltarfaB突变体侵袭HeLa细胞的能力低于野生型，且细胞内细菌的比例较低。对小鼠的竞争性感染表明，DeltarfaB突变体在宿主器官定殖方面存在缺陷，在粪便排泄中清除得更快。含有rfaB野生型等位基因的质粒（pRB3-rfaB）转化可部分挽救DeltarfaB突变体的缺陷。结果表明，负责向核心脂多糖添加糖基残基的RfaB有助于肠炎沙门氏菌肠炎血清型对去污剂的耐受性和毒力。
