Balance of inflammatory response in stable gingivitis and progressive periodontitis lesions
Balance of inflammatory response in stable gingivitis and progressive periodontitis lesions
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DOI：
10.1111/j.1365-2249.2006.03028.x
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发表时间：
2006-04-01
影响因子：
4.6
通讯作者：
Yamazaki, K
中科院分区：
文献类型：
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作者：
Honda, T;Domon, H;Yamazaki, K
炎症介质及其反调节分子之间的平衡可能是决定牙周病免疫病理结果的关键。根据临床和免疫学结果，稳定型牙周炎病变的免疫反应应该是平衡的，而进展型牙周炎病变的免疫反应偏向于促炎反应为主。然而，这一假设尚未得到证实。因此，本研究的目的是通过实时定量聚合酶链反应，比较牙龈炎和牙周炎病变中促炎因子和其他炎症分子等炎症介质和抗炎因子的基因表达谱。对于炎症介质，在牙周炎患者中，白细胞介素(IL)-1 β、干扰素(IFN)- γ和核因子受体激活剂(NF)- κ B配体倾向于升高，而肿瘤坏死因子(TNF)- α和IL-12 p40无差异。热休克蛋白60 （HSP60）在牙周炎中的表达明显上调。对于抗炎细胞因子，转化生长因子(TGF)- β 1在牙周炎中的表达高于牙龈炎，而IL-10和IL-4的表达无显著差异。这些发现进一步支持了我们之前的发现，即自身免疫对HSP60的反应可能在牙周炎病变中发挥作用，并提示细胞因子平衡的细微差异可能导致不同的疾病表达。
The balance between inflammatory mediators and their counter-regulatory molecules may be crucial for determining the outcome of immune pathology of periodontal diseases. Based on clinical and immunological findings, the immune response in stable gingivitis lesion is supposed to be in balance, whereas the response is skewed towards the predominance of proinflammatory reactivity in progressive periodontitis lesion. However, this hypothesis has not been verified. Therefore, the aim of this study was to compare the gene expression profile of inflammatory mediators including proinflammatory cytokines and other inflammatory molecules, and anti-inflammatory cytokines by using quantitative real-time polymerase chain reaction in gingivitis and periodontitis lesions showing distinct clinical entities. For inflammatory mediators, interleukin (IL)-1 beta, interferon (IFN)-gamma and receptor activator of nuclear factor (NF)-kappa B ligand tended to be higher in periodontitis, whereas tumour necrosis factor (TNF)-alpha and IL-12 p40 showed no difference. Heat-shock protein 60 (HSP60) expression was up-regulated significantly in periodontitis. For anti-inflammatory cytokines, transforming growth factor (TGF)-beta 1 expression tended to be higher in periodontitis compared with gingivitis, whereas no difference was observed for IL-10 and IL-4. These findings support further our previous finding that autoimmune response to HSP60 may exert in periodontitis lesion, and suggest that perhaps subtle differences in the balance of cytokines may result in different disease expression.