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首页> 外文期刊>Infection and immunity >Interaction of inflammatory cells and oral microorganisms. IV. In vitro release of lysosomal constituents from polymorphonuclear leukocytes exposed to supragingival and subgingival bacterial plaque.
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Interaction of inflammatory cells and oral microorganisms. IV. In vitro release of lysosomal constituents from polymorphonuclear leukocytes exposed to supragingival and subgingival bacterial plaque.

机译：炎症细胞与口腔微生物的相互作用。 IV。从暴露于龈上和龈下细菌菌斑的多形核白细胞中释放溶酶体成分。

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The deposition of bacterial plaques on tooth surfaces appears to be responsible for the initiation and progression of periodontal disease. In this study, human peripheral blood polymorphonuclear leukocytes (PMNs) actively released lysosomal constituents upon in vitro exposure to either viable or irradiated, supragingival or subgingival dental plaque. Plaques were obtained from the PMN donors (autologous plaque) or from pooled samples (homologous plaque) secured from patients with periodontal lesions. Fresh sera from PMN donors amplified the release reactions to supragingival and subgingival plaques. Heated (56 degrees C, 30 min) sera also enhanced release reactions, but not as consistently as fresh serum. It was postulated that modulation of PMN release by serum is mediated by complement components and/or antibodies to plaque bacteria. Electron microscopic observations indicated that degranulation and discharge of PMN lysosomal enzymes may be associated with phagocytosis of gram-positive and gram-negative plaque bacteria and with reverse endocytosis of lysosomes from cells contacting relatively large masses of aggregated plaque bacteria. These data suggest that PMN lysosome release in response to plaque may serve as a potential mechanism of tissue injury in the pathogenesis of gingival and periodontal inflammation.
机译：牙菌斑在牙齿表面的沉积似乎与牙周疾病的发生和发展有关。在这项研究中，人外周血多形核白细胞（PMN）在体外暴露于可行或辐射，龈上或龈下牙菌斑后，会主动释放溶酶体成分。从PMN供体（自体斑块）或从牙周病变患者固定的合并样品（同源斑块）中获得斑块。 PMN供体的新鲜血清放大了对龈上和龈下斑块的释放反应。加热（56摄氏度，30分钟）的血清也能增强释放反应，但不如新鲜血清稳定。据推测，血清对PMN释放的调节是由补体成分和/或抗噬菌体的抗体介导的。电子显微镜观察表明，PMN溶酶体酶的脱颗粒和释放可能与革兰氏阳性和革兰氏阴性菌斑噬菌体的吞噬作用以及与接触大量聚集菌斑细菌的细胞对溶酶体的逆向胞吞作用有关。这些数据表明，响应斑块的PMN溶酶体释放可能是牙龈和牙周炎发病机理中组织损伤的潜在机制。

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