Thakker M, Park J S, Carey V, Lee J C
Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA.
Infect Immun. 1998 Nov;66(11):5183-9. doi: 10.1128/IAI.66.11.5183-5189.1998.
Controversy persists over the role that the capsular polysaccharide plays in the pathogenesis of Staphylococcus aureus infections. To address this issue, we compared the mouse virulence of S. aureus Reynolds and capsule-defective mutant strains cultivated under conditions of high or low capsule expression. Strain Reynolds cells cultivated on Columbia salt agar plates expressed approximately 100-fold more type 5 capsular polysaccharide than did cells cultivated in Columbia salt broth. The relative virulence of strain Reynolds and its capsule-defective mutants after growth on either solid or liquid medium was examined in mice challenged intraperitoneally or intravenously. The results indicated that agar-grown Reynolds cells were cleared from the bloodstream of mice less readily than broth-grown Reynolds cells. When the parental and mutant strains were cultivated on solid medium, strain Reynolds sustained a higher level of bacteremia than did the capsular mutants. We performed in vitro opsonophagocytic killing assays to determine whether staphylococcal virulence for mice correlated with resistance to phagocytosis. S. aureus Reynolds cultivated on solid medium was susceptible to phagocytic killing only in the presence of specific capsular antibodies and complement. Strain Reynolds grown in broth showed opsonic requirements for phagocytic killing that were similar to those of the capsular mutants (grown in broth or on agar); i.e., the bacteria were opsonized for phagocytosis by nonimmune serum with complement activity. These studies indicate that optimal expression of capsule enhances bacterial virulence in the mouse model of bacteremia, probably by rendering the organisms resistant to opsonophagocytic killing by leukocytes.
关于荚膜多糖在金黄色葡萄球菌感染发病机制中所起的作用，争议仍然存在。为了解决这个问题，我们比较了在高或低荚膜表达条件下培养的金黄色葡萄球菌雷诺兹菌株和荚膜缺陷突变株对小鼠的毒力。在哥伦比亚盐琼脂平板上培养的雷诺兹菌株细胞表达的5型荚膜多糖比在哥伦比亚盐肉汤中培养的细胞多约100倍。在经腹腔或静脉注射攻击的小鼠中，检测了雷诺兹菌株及其荚膜缺陷突变株在固体或液体培养基上生长后的相对毒力。结果表明，琼脂培养的雷诺兹细胞比肉汤培养的雷诺兹细胞更不容易从小鼠血液中清除。当亲本菌株和突变菌株在固体培养基上培养时，雷诺兹菌株的菌血症水平高于荚膜突变株。我们进行了体外调理吞噬杀伤试验，以确定金黄色葡萄球菌对小鼠的毒力是否与对吞噬作用的抗性相关。在固体培养基上培养的金黄色葡萄球菌雷诺兹菌株仅在存在特异性荚膜抗体和补体的情况下易受吞噬杀伤。在肉汤中生长的雷诺兹菌株对吞噬杀伤的调理作用要求与荚膜突变株（在肉汤或琼脂上生长）相似；即，这些细菌被具有补体活性的非免疫血清调理以进行吞噬作用。这些研究表明，荚膜的最佳表达增强了小鼠菌血症模型中的细菌毒力，可能是通过使生物体对白细胞的调理吞噬杀伤产生抗性来实现的。
