Hu Dong-Liang, Cui Jing-Chun, Omoe Katsuhiko, Sashinami Hiroshi, Yokomizo Yuichi, Shinagawa Kunihiro, Nakane Akio
Department of Bacteriology, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8562, Japan.
Infect Immun. 2005 Jan;73(1):174-80. doi: 10.1128/IAI.73.1.174-180.2005.
Staphylococcal enterotoxin C (SEC), a bacterial superantigenic exotoxin, is commonly produced by invasive Staphylococcus aureus isolates, especially methicillin-resistant strains and isolates from animal diseases. We constructed and expressed a nontoxic mutant SEC (mSEC) and investigated whether immunization with mSEC, which is devoid of superantigenic activity, can protect against S. aureus infection. Mice were immunized with mSEC and challenged with viable S. aureus. The bacterial counts in the organs of mSEC-immunized mice were significantly lower and the survival rate was higher than the corresponding values for the control group. Immunization with mSEC strongly induced the production of T-helper 2 type antibodies, immunoglobulin G1, and immunoglobulin G2b. The production of interleukin-10 (IL-10) and IL-4 was significantly greater in immunized mice challenged with S. aureus than in the control mice, whereas the production of gamma interferon (IFN-gamma) was significantly decreased in the immunized mice. The cytokine response in a spleen cell culture that was stimulated with heat-killed S. aureus or SEC showed that immunization with mSEC inhibited IFN-gamma production and up-regulated IL-10 production in vitro. Furthermore, IFN-gamma and tumor necrosis factor alpha production in vitro was significantly inhibited by sera from mSEC-immunized mice but not by sera from control mice. These results suggest that immunization with mSEC devoid of superantigenic properties provides protection against S. aureus infection and that the protection might be mediated by SEC-specific neutralizing antibodies.
葡萄球菌肠毒素C(SEC)是一种细菌超抗原性外毒素,通常由侵袭性金黄色葡萄球菌分离株产生,尤其是耐甲氧西林菌株和来自动物疾病的分离株。我们构建并表达了一种无毒突变体SEC(mSEC),并研究了用缺乏超抗原活性的mSEC免疫是否能预防金黄色葡萄球菌感染。用mSEC免疫小鼠,然后用活的金黄色葡萄球菌进行攻击。mSEC免疫小鼠器官中的细菌计数显著低于对照组,存活率高于对照组。用mSEC免疫强烈诱导辅助性T2型抗体、免疫球蛋白G1和免疫球蛋白G2b的产生。用金黄色葡萄球菌攻击的免疫小鼠中白细胞介素-10(IL-10)和IL-4的产生显著高于对照小鼠,而免疫小鼠中γ干扰素(IFN-γ)的产生显著降低。用热灭活的金黄色葡萄球菌或SEC刺激的脾细胞培养中的细胞因子反应表明,用mSEC免疫在体外抑制IFN-γ的产生并上调IL-10的产生。此外,mSEC免疫小鼠的血清显著抑制体外IFN-γ和肿瘤坏死因子α的产生,但对照小鼠的血清则无此作用。这些结果表明,用缺乏超抗原特性的mSEC免疫可预防金黄色葡萄球菌感染,并且这种保护作用可能由SEC特异性中和抗体介导。