Bodet C, Chandad F, Grenier D
Groupe de Recherche en Ecologie Buccale, Faculté de Médecine Dentaire, Université Laval, Quebec City, Quebec, Canada.
Clin Exp Immunol. 2006 Jan;143(1):50-7. doi: 10.1111/j.1365-2249.2005.02956.x.
Periodontitis is characterized by an accumulation of inflammatory cells in periodontal tissue and subgingival sites. Leukocytes play a major role in the host response to Porphyromonas gingivalis, a major aetiological agent of chronic periodontitis. Secretion of high levels of inflammatory mediators, including cytokines and prostaglandins, by leucocytes is believed to contribute to periodontal tissue destruction. The aim of this study was to investigate the inflammatory response of an ex vivo whole blood model to P. gingivalis stimulation. The production of interleukin-1 beta (IL-1beta), IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor alpha (TNF-alpha), interferon gamma (IFN-gamma), IFN-gamma-inducible protein 10 (IP-10), monocyte chemoattractant protein-1 (MCP-1), Regulated on Activation Normal T cell Expressed and Secreted (RANTES) and prostaglandin E2 (PGE2) were quantified by enzyme-linked immunosorbent assays. P. gingivalis induced the secretion of the pro-inflammatory cytokines IL-1beta, TNF-alpha, IL-6 and IFN-gamma, the chemokines IL-8, RANTES and MCP-1 and the inflammatory mediator PGE2 in an ex vivo human whole blood model. The secretion levels were dependent on the strain and the infectious dose used. While the mediator profiles were comparable between six healthy subjects, a high interindividual variability in the levels of secreted mediators was observed. This study supports the view that P. gingivalis, by inducing high levels of inflammatory mediators from a mixed leucocyte population, can contribute to the progression of periodontitis.
牙周炎的特征是牙周组织和龈下部位出现炎症细胞积聚。白细胞在宿主对牙龈卟啉单胞菌（慢性牙周炎的主要病原体）的反应中起主要作用。白细胞分泌高水平的炎症介质，包括细胞因子和前列腺素，被认为会导致牙周组织破坏。本研究的目的是调查体外全血模型对牙龈卟啉单胞菌刺激的炎症反应。通过酶联免疫吸附测定法定量白细胞介素 -1β（IL -1β）、IL -4、IL -5、IL -6、IL -8、IL -10、IL -12p70、IL -13、肿瘤坏死因子α（TNF -α）、干扰素γ（IFN -γ）、IFN -γ诱导蛋白10（IP -10）、单核细胞趋化蛋白 -1（MCP -1）、活化正常T细胞表达和分泌调节因子（RANTES）以及前列腺素E2（PGE2）的产生。在体外人全血模型中，牙龈卟啉单胞菌诱导促炎细胞因子IL -1β、TNF -α、IL -6和IFN -γ、趋化因子IL -8、RANTES和MCP -1以及炎症介质PGE2的分泌。分泌水平取决于所用的菌株和感染剂量。虽然六个健康受试者之间的介质谱具有可比性，但观察到分泌介质水平存在高度个体间差异。本研究支持这样的观点，即牙龈卟啉单胞菌通过从混合白细胞群体中诱导高水平炎症介质，可促进牙周炎的进展。
