Wessels M R, Rubens C E, Benedí V J, Kasper D L
Channing Laboratory, Brigham and Women's Hospital, Boston, MA 02115.
Proc Natl Acad Sci U S A. 1989 Nov;86(22):8983-7. doi: 10.1073/pnas.86.22.8983.
Sialylation of bacterial capsules has been proposed as an important virulence factor for several species of encapsulated pathogens, including group B Streptococcus. We have constructed a transposon mutant strain of type III group B Streptococcus that expresses a capsular polysaccharide differing from the wild type only in that the mutant strain's capsule lacks sialic acid. The mutant polysaccharide is antigenically identical to the capsular polysaccharide of type 14 Streptococcus pneumoniae, as predicted by the structures of the type III group B Streptococcus and S. pneumoniae polysaccharides. Loss of capsular sialic acid was associated with loss of virulence in the mutant strain in a neonatal rat model of lethal group B Streptococcus infection. These studies demonstrate directly that capsular sialic acid is a critical virulence determinant for type III group B Streptococcus and support the general hypothesis that surface sialylation aids pathogenic microorganisms in evading host defenses.
细菌荚膜的唾液酸化已被认为是包括B族链球菌在内的几种有荚膜病原体的重要毒力因子。我们构建了III型B族链球菌的转座子突变株,该突变株表达的荚膜多糖与野生型的不同之处仅在于突变株的荚膜缺乏唾液酸。如III型B族链球菌和肺炎链球菌多糖的结构所预测的那样,突变多糖在抗原性上与14型肺炎链球菌的荚膜多糖相同。在致死性B族链球菌感染的新生大鼠模型中,突变株荚膜唾液酸的缺失与毒力丧失有关。这些研究直接证明荚膜唾液酸是III型B族链球菌的关键毒力决定因素,并支持表面唾液酸化有助于致病微生物逃避宿主防御的一般假说。