Ashkenazi M, White R R, Dennison D K
Department of Periodontics, University of Texas Health Science Center, Houston.
J Periodontal Res. 1992 Sep;27(5):457-65. doi: 10.1111/j.1600-0765.1992.tb01818.x.
Compromised neutrophil function has been found in a number of patients with localized juvenile periodontitis (LJP), although the pathogenic mechanism is unknown. Since infection with Actinobacillus actinomycetemcomitans is frequently found in patients with LJP, we have evaluated in vitro the effect of a bacterial extract of A. actinomycetemcomitans on the development of the respiratory burst by neutrophils. Pre-incubation of neutrophils with bacterial extract increased H2O2 induced by FMLP and zymosan in a dose-dependent fashion. Substitution of FMLP for bacterial extract produced similar results. Moreover, FMLP and bacterial extract had an additive effect on superoxide production following phagocytosis of zymosan. In contrast, bacterial extract significantly decreased PMA-stimulated H2O2, but pre-incubation with FMLP instead of bacterial extract failed to decrease PMA-stimulated H2O2. Bacterial extract did not change the percentage of cells activated by FMLP, opsonized zymosan, or PMA. Heat-treated bacterial extract induced effects similar to non-treated extract. Bacterial extract treated with proteinase K or phenol extraction increased FMLP or zymosan stimulated H2O2 equivalent to non-treated bacterial extract. In contrast, proteinase K or phenol extraction abolished the inhibitory effect of bacterial extract on PMA-stimulated H2O2 production. The bacterial extract component(s) that inhibits PMA-stimulated H2O2 is therefore a protein(s), resistant to 56 degrees C, and is not endotoxin. The partially activated state of PMNs exposed to A. actinomycetemcomitans extract, combined with their reduced ability to respond to a protein kinase C-dependent stimulus, may partially explain the abnormalities noted in LJP patients.
尽管致病机制尚不清楚，但在许多局限性青少年牙周炎（LJP）患者中发现了中性粒细胞功能受损。由于在LJP患者中经常发现伴放线放线杆菌感染，我们在体外评估了伴放线放线杆菌的细菌提取物对中性粒细胞呼吸爆发发展的影响。用细菌提取物预孵育中性粒细胞以剂量依赖的方式增加了由FMLP和酵母聚糖诱导的H2O2。用细菌提取物替代FMLP产生了类似的结果。此外，FMLP和细菌提取物对酵母聚糖吞噬后超氧化物的产生具有相加作用。相反，细菌提取物显著降低了PMA刺激的H2O2，但用FMLP而非细菌提取物预孵育未能降低PMA刺激的H2O2。细菌提取物没有改变由FMLP、调理酵母聚糖或PMA激活的细胞百分比。热处理的细菌提取物诱导的效应与未处理的提取物相似。用蛋白酶K或酚提取处理的细菌提取物增加了FMLP或酵母聚糖刺激的H2O2，相当于未处理的细菌提取物。相反，蛋白酶K或酚提取消除了细菌提取物对PMA刺激的H2O2产生的抑制作用。因此，抑制PMA刺激的H2O2的细菌提取物成分是一种对56℃有抗性的蛋白质，且不是内毒素。暴露于伴放线放线杆菌提取物的中性粒细胞的部分激活状态，加上它们对蛋白激酶C依赖性刺激反应能力的降低，可能部分解释了LJP患者中观察到的异常情况。
