Department of Medicine, Albert Einstein College of Medicine and Montefiore Medical Center, New York, New York 10461, USA.
J Clin Invest. 2010 Sep;120(9):3099-102. doi: 10.1172/JCI44312. Epub 2010 Aug 25.
The appearance of methicillin-resistant Staphylococcus aureus (MRSA) as an endemic microbe, first in hospital and health care settings and more recently in the community, has led to a disastrous situation in which use of the available antibiotic armamentarium is increasingly ineffective and spawns further antibiotic resistance. This vicious cycle highlights the pressing need for an S. aureus vaccine. However, to date, clinical trials with S. aureus vaccines have not demonstrated sustained efficacy. In this issue of the JCI, Skurnik and colleagues report that specific antibodies to two different S. aureus surface polysaccharides, which independently promote effector cell killing of S. aureus in vitro and protection against S. aureus in animal models, bind to and abrogate the activity of one another when they are combined. This fascinating finding suggests a new paradigm to explain the failure of antibody immunity to S. aureus.
耐甲氧西林金黄色葡萄球菌（MRSA）作为一种地方性微生物的出现，最初在医院和医疗保健环境中，最近在社区中，导致了一种灾难性的情况，即现有的抗生素武器库的使用越来越无效，并产生了进一步的抗生素耐药性。这种恶性循环突出了迫切需要开发金黄色葡萄球菌疫苗。然而，迄今为止，金黄色葡萄球菌疫苗的临床试验并未显示出持续的疗效。在本期 JCI 中，Skurnik 及其同事报告称，针对两种不同金黄色葡萄球菌表面多糖的特异性抗体，它们在体外独立促进效应细胞杀伤金黄色葡萄球菌，并在动物模型中保护免受金黄色葡萄球菌的侵害，当它们结合在一起时，会相互结合并消除彼此的活性。这一引人入胜的发现提出了一个新的范例，用以解释金黄色葡萄球菌抗体免疫的失败。
