Ashkenazi M, White R R, Dennison D K
Department of Periodontics, Dental Branch University of Texas Health Science Center, Houston.
J Periodontal Res. 1992 Jul;27(4 Pt 1):264-73. doi: 10.1111/j.1600-0765.1992.tb01677.x.
Localized juvenile periodontitis is an early onset periodontitis, usually localized to molars and incisors. Patients usually present with decreased chemotaxis of systemic neutrophils (PMNs) and infection with Actinobacillus actinomycetemcomitans. The pathogenic mechanisms involved have not been clarified. The purpose of this study was to determine if an extract of A. actinomycetemcomitans could induce changes in PMN chemotaxis similar to those reported in LJP patients. It was demonstrated that the bacterial extract was chemotactic for neutrophils. When neutrophils were pre-incubated with the bacterial extract, chemotaxis toward zymosan-activated serum, FMLP and the bacterial extract was inhibited in two different chemotaxis assays (Boyden chamber and under-agarose). Bacterial extract had no effect on random migration in either assay. Pre-incubation with the extract induced increased expression of CD11b/CD18 (Mac-1), Gp110, and FMLP receptors and increased F-actin polymerization following FMLP or PMA stimulation compared to cells not treated with the extract. Treatment of the bacterial extract with proteinase K or phenol extraction reversed the PMN chemotaxis inhibition activity, but increased significantly the random migration of PMNs. Heating the bacterial extract to 56 degrees C had no effect on its activity. The component(s) in the bacterial extract that inhibits chemotaxis is therefore a protein(s), not sensitive to 56 degrees C, and is not endotoxin. This study suggests that A. actinomycetemcomitans may contribute to the pathogenesis of localized juvenile periodontitis by inhibiting chemotaxis. Interference with chemotaxis by A. actinomycetemcomitans, however, occurs through a mechanism other than inhibition of actin assembly, reduction of CD11b/CD18 or Gp110 expression, or blockage/downregulation of FMLP receptors.
局限性青少年牙周炎是一种早发性牙周炎，通常局限于磨牙和切牙。患者通常表现为全身中性粒细胞（PMN）趋化性降低以及伴放线放线杆菌感染。其中涉及的致病机制尚未阐明。本研究的目的是确定伴放线放线杆菌提取物是否能诱导PMN趋化性发生类似于局限性青少年牙周炎患者所报道的变化。结果表明，该细菌提取物对中性粒细胞具有趋化作用。当中性粒细胞与细菌提取物预孵育后，在两种不同的趋化性检测方法（Boyden小室法和琼脂糖下法）中，其对酵母聚糖激活血清、FMLP和细菌提取物的趋化性均受到抑制。在任一检测方法中，细菌提取物对随机迁移均无影响。与未用提取物处理的细胞相比，预孵育提取物可诱导CD11b/CD18（Mac-1）、Gp110和FMLP受体的表达增加，以及在FMLP或PMA刺激后F-肌动蛋白聚合增加。用蛋白酶K处理细菌提取物或进行酚抽提可逆转PMN趋化性抑制活性，但显著增加了PMN的随机迁移。将细菌提取物加热至56℃对其活性无影响。因此，细菌提取物中抑制趋化性的成分是一种蛋白质，对56℃不敏感，且不是内毒素。本研究提示，伴放线放线杆菌可能通过抑制趋化性而参与局限性青少年牙周炎的发病机制。然而，伴放线放线杆菌对趋化性的干扰是通过一种不同于抑制肌动蛋白组装、降低CD11b/CD18或Gp110表达，或阻断/下调FMLP受体的机制发生的。
