Bryant Amy E, Bayer Clifford R, Huntington Jeremy D, Stevens Dennis L
Veterans Affairs Medical Center, Boise, Idaho 83702, USA.
J Infect Dis. 2006 Jun 15;193(12):1685-92. doi: 10.1086/504261. Epub 2006 May 10.
Necrotizing fasciitis and myonecrosis caused by invasive infection with group A streptococci (GAS) are life-threatening conditions that have reemerged worldwide. Half of all GAS myonecrosis cases have no known portal of entry; yet, for unknown reasons, infection becomes established precisely at the site of a prior, nonpenetrating minor injury, such as a muscle strain. We hypothesized that GAS establishes infection by binding to surface molecules that are up-regulated on injured skeletal-muscle cells. Here, we isolated and identified vimentin as the major skeletal-muscle GAS-binding protein. Furthermore, we found that vimentin expression was up-regulated on injured skeletal-muscle cells in vitro and was expressed in muscle tissues from a patient with GAS myonecrosis who died of streptococcal toxic shock syndrome. These findings provide a molecular mechanism to explain the development of severe GAS soft-tissue infections at the sites of prior minor muscle trauma. This understanding may provide a basis for novel preventive strategies or therapies for patients with this devastating infection.
A 组链球菌(GAS)侵入性感染引起的坏死性筋膜炎和肌坏死是全球范围内再度出现的危及生命的病症。所有 GAS 肌坏死病例中有一半没有已知的感染入口;然而,出于未知原因,感染恰恰在先前非穿透性轻微损伤(如肌肉拉伤)的部位确立。我们推测 GAS 通过与损伤的骨骼肌细胞上上调的表面分子结合来确立感染。在此,我们分离并鉴定波形蛋白为主要的骨骼肌 GAS 结合蛋白。此外,我们发现波形蛋白在体外损伤的骨骼肌细胞上表达上调,并且在死于链球菌中毒性休克综合征的 GAS 肌坏死患者的肌肉组织中也有表达。这些发现提供了一种分子机制,以解释先前轻微肌肉创伤部位严重 GAS 软组织感染的发生发展。这一认识可能为患有这种毁灭性感染的患者提供新的预防策略或治疗方法的基础。