Salvi Giovanni E, Spets-Happonen Satu, Singer Robert E, Offenbacher Steven
Department of Periodontology & Fixed Prosthodontics, University of Berne, School of Dental Medicine, Berne, Switzerland.
J Periodontol. 2005 Jan;76(1):16-21. doi: 10.1902/jop.2005.76.1.16.
The purpose of this study was to determine whether lymphocytic cells regulate the monocytic hyperinflammatory trait (MO+) in chronic periodontitis patients. Using a P. gingivalis challenge model in severe combined immunodeficient (SCID) mice, we tested the effects of adoptively transferred human peripheral blood leukocytes from gingivitis and chronic periodontitis diabetic and non-diabetic individuals on monocytic responses.
This response was examined using the subcutaneous tissue chamber infection model. Three weeks following cell reconstitution, all SCID mice were challenged with 10(9) colony forming units of live P. gingivalis HG405. Chamber contents were collected at day 7 after bacterial challenge for prostaglandin E2 (PGE2) analysis and chamber rejection monitored up to day 30. Gingival crevicular fluid (GCF) samples were collected from all patients for PGE2 analysis. Both chamber fluid- and GCF-PGE2 levels were determined by enzyme-linked immunosorbent assays (ELISA).
Significantly elevated GCF-PGE2 levels were found in diabetic as well as in non-diabetic patients with moderate/advanced periodontitis compared to diabetic and non-diabetic subjects with gingivitis/mild periodontitis at P= 0.01 and P= 0.001, respectively. As reflected in chamber fluid PGE2 levels and percentage chamber rejection, lymphocytic sensitization to P. gingivalis occurred in both diabetics and non-diabetics with moderate/advanced periodontitis, but not in diabetics and non-diabetics with gingivitis/mild periodontitis.
These results suggest that the exaggerated monocytic inflammatory response trait (MO+) associated with moderate/advanced chronic periodontitis is due, at least in part, to lymphocytic modulation, while the directional findings for lymphocytes from diabetic subjects deserve further investigation. Our findings further demonstrate that the SCID mouse model is a useful animal model to study human immune responses to periodontal microorganisms.
本研究旨在确定淋巴细胞是否调节慢性牙周炎患者的单核细胞高炎症特征(MO+)。我们在严重联合免疫缺陷(SCID)小鼠中使用牙龈卟啉单胞菌攻击模型,测试了来自牙龈炎和慢性牙周炎糖尿病及非糖尿病个体的过继转移人外周血白细胞对单核细胞反应的影响。
使用皮下组织腔感染模型检测这种反应。细胞重建三周后,所有SCID小鼠用10⁹个牙龈卟啉单胞菌HG405活菌落形成单位进行攻击。在细菌攻击后第7天收集腔内容物进行前列腺素E2(PGE2)分析,并监测腔排斥直至第30天。从所有患者收集龈沟液(GCF)样本进行PGE2分析。通过酶联免疫吸附测定(ELISA)测定腔液和GCF中的PGE2水平。
与患有牙龈炎/轻度牙周炎的糖尿病和非糖尿病受试者相比,患有中度/重度牙周炎的糖尿病和非糖尿病患者的GCF-PGE2水平显著升高,P值分别为0.01和0.001。如腔液PGE2水平和腔排斥百分比所示,患有中度/重度牙周炎的糖尿病和非糖尿病患者对牙龈卟啉单胞菌发生了淋巴细胞致敏,但患有牙龈炎/轻度牙周炎的糖尿病和非糖尿病患者未发生。
这些结果表明,与中度/重度慢性牙周炎相关的单核细胞炎症反应特征(MO+)增强至少部分归因于淋巴细胞调节,而糖尿病受试者淋巴细胞的定向研究结果值得进一步研究。我们的研究结果进一步证明,SCID小鼠模型是研究人类对牙周微生物免疫反应的有用动物模型。