Brissette Catherine A, Lukehart Sheila A
Department of Pathobiology, University of Washington, Seattle, Washington 98195, USA.
Infect Immun. 2002 Jul;70(7):3982-4. doi: 10.1128/IAI.70.7.3982-3984.2002.
Spirochetes, including Treponema denticola, are implicated in the pathogenesis of periodontal disease. Because T. denticola lacks lipopolysaccharides that serve as targets for human beta-defensin (h beta D) binding, we postulated that T. denticola would resist killing by h beta D. We showed that T. denticola is resistant to h beta D-1 and -2. Protease inhibitors did not enhance killing of T. denticola by h beta D-2, suggesting that degradation of h beta D-2 by treponemal proteases is not a major factor in T. denticola resistance.
包括齿垢密螺旋体在内的螺旋体与牙周疾病的发病机制有关。由于齿垢密螺旋体缺乏作为人类β-防御素(hβD)结合靶点的脂多糖,我们推测齿垢密螺旋体能够抵抗hβD的杀伤作用。我们发现齿垢密螺旋体对hβD-1和-2具有抗性。蛋白酶抑制剂并不能增强hβD-2对齿垢密螺旋体的杀伤作用,这表明密螺旋体蛋白酶对hβD-2的降解不是齿垢密螺旋体产生抗性的主要因素。