Platelet activation and platelet–leukocyte interaction in generalized aggressive periodontitis
Platelet activation and platelet–leukocyte interaction in generalized aggressive periodontitis
复制标题
DOI：
10.1189/jlb.4a1115-526rr
复制
发表时间：
2016-11
影响因子：
5.5
通讯作者：
Y. Zhan;R. Lu;H. Meng;Xiane Wang;J. Hou
中科院分区：
文献类型：
--
作者：
Y. Zhan;R. Lu;H. Meng;Xiane Wang;J. Hou
广泛性侵袭性牙周炎（GAgP）是宿主对细菌攻击反应的炎症性疾病。为了探讨血小板在牙周炎患者宿主-微生物相互作用中的作用，纳入了 124 名 GAgP 患者和 57 名健康受试者。 GAgP 组亚临床血小板功能状态的可靠指标、血小板计数 (PLT)、血小板大细胞比 (PLCR) 和平均血小板体积 (MPV) 均显着低于对照组，且与临床牙周参数呈负相关。与健康受试者相比，GAgP 患者中性粒细胞中重要的胞质蛋白、血浆中的钙卫蛋白 (S100A8/A9) 和龈沟液 (GCF) 的水平显着升高。此外，GCF钙卫蛋白水平与PLCR和MPV值呈负相关。为了探讨牙周炎中血小板指数变化的可能机制，进行了流式细胞术分析，发现GAgP患者与健康对照相比具有更高的血小板活化状态。牙龈卟啉单胞菌 (P. gingivalis) 和重组人 S100A8/A9 (rhS100A8/A9) 诱导健康受试者全血中的血小板活化并促进血小板-白细胞聚集体形成。与健康受试者相比，针对牙龈卟啉单胞菌和 rhS100A8/A9，GAgP 患者的血小板活化增加，血小板-白细胞聚集体的形成增加。在 GAgP 患者的牙龈组织上发现了血小板聚集体和附着在白细胞上的血小板，这表明循环中血小板大小和计数的减少可能与发炎牙龈处大的活化血小板的消耗有关。血小板在宿主对牙周感染的反应中可能具有以前未被认识到的作用。
Generalized aggressive periodontitis (GAgP) is an inflammatory disease of host response to bacterial challenge. To explore the role of platelets in host–microbial interactions in patients with periodontitis, 124 patients with GAgP and 57 healthy subjects were enrolled. Reliable indicators of subclinical platelet functional status, platelet count (PLT), platelet large cell ratio (PLCR), and mean platelet volume (MPV), were significantly lower in the GAgP group than in the control group and were negatively correlated with clinical periodontal parameters. The levels of important cytosolic protein in neutrophils, calprotectin (S100A8/A9) in plasma, and gingival crevicular fluid (GCF) were significantly higher in patients with GAgP compared with healthy subjects. Moreover, the GCF calprotectin level was negatively correlated with PLCR and MPV values. To explore the possible mechanisms of changes in platelet indices in periodontitis, flow cytometry analysis was performed, and patients with GAgP were found to have a higher status of platelet activation compared with healthy controls. Porphyromonas gingivalis (P. gingivalis) and recombinant human S100A8/A9 (rhS100A8/A9) induced platelet activation and facilitated platelet–leukocyte aggregate formation in whole blood of healthy subjects. In response to P. gingivalis and rhS100A8/A9, platelets from patients with GAgP increased activation and increased formation of platelet–leukocyte aggregates compared with those from healthy subjects. Platelet aggregates and platelets attached to leukocytes were found on gingival tissues from patients with GAgP, suggesting that decreased platelet size and count in the circulation might be related to consumption of large, activated platelets at inflamed gingiva. Platelets may have a previously unrecognized role in host response to periodontal infection.