Autoantibodies to beta1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger prostaglandin E2 generation.
Autoantibodies to beta1-adrenoceptors in human chronic periodontitis induce overexpression of fibroblast CD40 and trigger prostaglandin E2 generation.
复制标题
人类慢性牙周炎中β1-肾上腺素受体的自身抗体诱导成纤维细胞CD40过度表达并触发前列腺素E2的产生。
DOI：
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发表时间：
2009
影响因子：
3.5
通讯作者：
E. Borda
中科院分区：
文献类型：
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作者：
L. Sterin‐Borda;C. Furlán;E. Borda
背景与目的
自身免疫机制可能参与牙周病的发病机制。研究了自身抗体结合和激活人牙龈成纤维细胞的β（1）-肾上腺素受体（β（1）-AR）的潜力，以提供慢性牙周病体液免疫反应改变的证据。
材料和方法
采用流式细胞术和酶联免疫吸附试验（ELISA）检测血清抗体，其中使用细胞培养贴壁牙龈成纤维细胞和/或其纯化膜和/或对应于人β（1）-AR第二环的合成肽。同时检测慢性牙周病患者抗体对PGE（2）生成和CD 40表达的影响。
结果
来自慢性牙周病患者的循环免疫球蛋白G（IgG）（而不是来自正常个体）与成纤维细胞表面相互作用，激活β（1）-AR。阿替洛尔或CGP 20712（β 1-AR拮抗剂）和β 1合成肽抑制IgG与β 1-AR的相互作用。来自慢性牙周病患者的免疫球蛋白G也显示出与特异性β 1-AR激活相关的激动剂样活性，增加PGE 2生成和CD 40过表达。相应的亲和纯化的抗β（1）-AR肽IgG模拟这些效果。这两种作用都可以通过抑制环氧合酶来防止。
结论
这篇文章支持体液免疫改变参与慢性牙周病导致突触后功能失调。抗体-β（1）-AR相互作用可诱导促炎介质（PGE（2）和CD 40表达）的过度产生。PGE（2）-CD 40-IgG轴可能在慢性牙周病炎症过程的病理生理机制中起作用。
BACKGROUND AND OBJECTIVE
Autoimmune mechanisms may contribute to the pathogenesis of periodontal disease. Autoantibodies with the potential to bind and activate beta(1)-adrenoceptors (beta(1)-AR) of human gingival fibroblasts were studied to provide evidence of altered humoral immune response in chronic periodontal disease.
MATERIAL AND METHODS
Flow cytometry and enzyme-linked immunosorbent assay using cell culture-adherent gingival fibroblasts and/or their purified membranes and/or a synthetic peptide corresponding to the second extracellular loop of human beta(1)-AR were used to detect serum antibodies. The effects of antibodies from chronic periodontal disease patients on PGE(2) generation and CD40 expression were also tested.
RESULTS
Circulating immunoglobulin G (IgG) from chronic periodontal disease patients (but not from normal individuals) interacted with the fibroblast surface, activating beta(1)-AR. Atenolol or CGP 20712 (beta 1-AR antagonists) and beta(1) synthetic peptide inhibited the interaction of IgG with beta(1)-AR. Immunoglobulin G from chronic periodontal disease patients also displayed agonist-like activity associated with specific beta(1)-AR activation, increasing PGE(2) generation and CD40 overexpression. The corresponding affinity-purified anti-beta(1)-AR peptide IgG mimicked these effects. Both effects were prevented by inhibition of cyclo-oxygenase.
CONCLUSION
This article supports the participation of humoral immune alterations in chronic periodontal disease resulting in postsynaptic functional deregulation. Overproduction of proinflammatory mediators (PGE(2) and CD40 expression) is induced as a consequence of antibody-beta(1)-AR interaction. The PGE(2)-CD40-IgG axis may play a part in the pathophysiological mechanisms underlying the inflammatory process in chronic periodontal disease.
CD40 介导牙龈和牙周膜成纤维细胞的激活。
影响因子：
4.3
作者：
Sempowski,GD;Chess,PR;Moretti,AJ;Padilla,J;Phipps,RP;Blieden,TM
通讯作者：
Blieden,TM
CD40 是正常人肺成纤维细胞上的功能激活抗原和 B7 独立 T 细胞共刺激分子。
DOI：
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发表时间：
1997
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Sempowski,GD;Chess,PR;Phipps,RP
通讯作者：
Phipps,RP
影响因子：
3.5
作者：
Phipps, RP;Borrello, MA;Blieden, TM
通讯作者：
Blieden, TM