Darmstadt G L, Fleckman P, Rubens C E
Divisions of Infectious Diseases, Department of Pediatrics, Division of Dermatology, University of Washington School of Medicine, Seattle, WA, USA.
J Infect Dis. 1999 Nov;180(5):1718-21. doi: 10.1086/315066.
We hypothesized that the primary epidermal cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1alpha, which are produced after skin injury, modulate bacterial adherence and the initiation of group A streptococcal skin infections. Streptococcus pyogenes binds preferentially to highly differentiated keratinocytes in vitro, simulating the superficial human skin infection, impetigo, and providing a model system for testing this hypothesis. Exposure of keratinocytes to 10 ng/mL TNF-alpha for 20 h decreased adherence to undifferentiated and differentiated keratinocytes by 33% and 38%, respectively. Treatment with 1 ng/mL IL-1alpha decreased adherence to undifferentiated and differentiated keratinocytes by 23% and 18%, respectively. Exposure to both cytokines simultaneously produced an additive 50% reduction in adherence. These data suggest that TNF-alpha and IL-1alpha may play a role in cutaneous host defense by impeding streptococcal adherence and decreasing its ability to form a nidus of infection in the skin.
我们推测，皮肤损伤后产生的主要表皮细胞因子，即肿瘤坏死因子（TNF）-α和白细胞介素（IL）-1α，可调节细菌黏附以及A组链球菌皮肤感染的起始。化脓性链球菌在体外优先结合高度分化的角质形成细胞，模拟人类浅表皮肤感染脓疱病，并提供了一个用于检验该假设的模型系统。角质形成细胞暴露于10 ng/mL TNF-α 20小时后，对未分化和分化角质形成细胞的黏附分别降低了33%和38%。用1 ng/mL IL-1α处理后，对未分化和分化角质形成细胞的黏附分别降低了23%和18%。同时暴露于两种细胞因子会使黏附额外降低50%。这些数据表明，TNF-α和IL-1α可能通过阻碍链球菌黏附并降低其在皮肤中形成感染灶的能力，在皮肤宿主防御中发挥作用。
