Department of Rheumatology and Inflammation Research, Institute of Medicine, University of Gothenburg. Sweden.
J Infect Dis. 2013 Sep;208(6):990-9. doi: 10.1093/infdis/jit288. Epub 2013 Jun 24.
Skin infections are frequently caused by Staphylococcus aureus and can lead to a fatal sepsis. The microbial mechanisms controlling the initiation and progression from mild skin infection to a severe disseminated infection remain poorly understood. Using a combination of clinical data and in vitro and ex vivo assays, we show that staphylokinase, secreted by S. aureus, promoted the establishment of skin infections in humans and increased bacterial penetration through skin barriers by activating plasminogen. However, when infection was established, the interaction between staphylokinase and plasminogen did not promote systemic dissemination but induced the opening and draining of abscesses and decreased disease severity in neutropenic mice. Also, increased staphylokinase production was associated with noninvasive S. aureus infections in patients. Our results point out the dual roles of staphylokinase in S. aureus skin infections as promoting the establishment of infections while decreasing disease severity.
皮肤感染通常由金黄色葡萄球菌引起，并可能导致致命的败血症。控制由轻度皮肤感染向严重播散性感染的起始和进展的微生物机制仍知之甚少。我们使用临床数据以及体外和离体检测的组合，显示金黄色葡萄球菌分泌的葡激酶促进了人类皮肤感染的建立，并通过激活纤溶酶原增加了细菌对皮肤屏障的穿透。然而，当感染建立后，葡激酶与纤溶酶原之间的相互作用并未促进全身性播散，而是诱导脓肿的开放和引流，并降低中性粒细胞减少小鼠的疾病严重程度。此外，葡激酶产量的增加与患者的非侵袭性金黄色葡萄球菌感染有关。我们的结果指出了葡激酶在金黄色葡萄球菌皮肤感染中的双重作用，既促进感染的建立，又降低疾病的严重程度。
