Role of anti-β1 adrenergic antibodies from patients with periodontitis in cardiac dysfunction.
Role of anti-β1 adrenergic antibodies from patients with periodontitis in cardiac dysfunction.
复制标题
牙周炎患者抗β1肾上腺素能抗体在心功能障碍中的作用。
DOI：
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发表时间：
2012
影响因子：
3.3
通讯作者：
L. Sterin‐Borda
中科院分区：
文献类型：
--
作者：
M. Segovia;Sabrina Ganzinelli;S. Reina;E. Borda;L. Sterin‐Borda
背景
牙周炎患者牙龈成纤维细胞中β 1肾上腺素受体（β 1-AR）自身抗体的存在抑制了原代细胞特异性生长并诱导促炎介质的过度表达。牙周炎患者血清中β 1-AR自身抗体与心肌反应并改变心肌收缩力。还研究了血清β（1）-AR自身抗体的存在与心率变异性（HRV）改变之间的关系。
方法
采用酶联免疫吸附试验（ELISA），使用心脏和牙龈成纤维细胞膜或对应于人β（1）-AR第二胞外环的合成肽检测血清自身抗体。根据22：00至08：00生成的RR间期文件评估HRV。在自发的大鼠离体心房上测量自身抗体对收缩力的影响。
结果
来自36名牙周炎患者和20名健康个体（对照）的循环自身抗体与成纤维细胞、心脏表面和β（1）-AR合成肽相互作用。抗牙龈膜抗体、抗心肌膜抗体和β 1-AR合成肽抗体的阳性率分别为88.8%、77.7%和92.8%。在血清β 1-AR合成肽阳性的牙周炎患者中，88.5%的患者心率变异性降低。相应的亲和纯化的抗β（1）-AR肽IgG显示部分激动剂样活性，改变离体心房收缩力。
结论
本文描述了牙周炎患者血清中具有抗β（1）-AR活性的IgG水平升高。这些患者表现为心率减慢，其血清来源的IgG诱导了心房的异常收缩。我们认为，牙周炎增加心血管疾病的风险，虽然它增加抗β（1）-AR自身抗体，改变心肌收缩力。
BACKGROUND
The presence of serum autoantibodies against β(1) adrenoreceptors (β(1)-ARs) in human gingival fibroblast from patients with periodontitis inhibits primary cell-specific growth and induces over-expression of pro-inflammatory mediators. Serum β(1)-AR autoantibodies from patients with periodontitis react with myocardium and modify cardiac contractility. The relationship between the presence of serum β(1)-AR autoantibodies and alterations in heart rate variability (HRV) was also studied.
METHODS
An enzyme-linked immunosorbent assay (ELISA) using cardiac and gingival fibroblast membranes or synthetic peptides corresponding to the second extracellular loop of human β(1)-AR was used to detect serum autoantibodies. The HRV was assessed from RR interval files generated from 22:00 to 08:00 hours. The autoantibody effects on contractility were measured on spontaneous rat isolated atria.
RESULTS
Circulating autoantibodies from 36 patients with periodontitis and 20 healthy individuals (controls) interacted with fibroblasts, the cardiac surface, and β(1)-AR synthetic peptides. The distributions of serum antibodies against gingival and myocardium membranes and β(1)-AR synthetic peptide were 88.8%, 77.7%, and 92.8%, respectively. Moreover, 88.5% of patients with periodontitis whose sera were positive against β(1)-AR synthetic peptide had decreased HRV. The corresponding affinity-purified anti-β(1)-AR peptide IgG displayed partial agonist-like activity modifying the isolated atria contractility.
CONCLUSION
This manuscript describes that patients with periodontitis showed increased levels of serum IgG with reactive activity against β(1)-AR. Those patients demonstrated decrease in heart rate, and IgG derived from their sera induced aberrant contractility of heart atrium. We propose that periodontitis increases the risk of cardiovascular diseases, although it increases anti-β(1)-AR autoantibody that alters myocardial contractility.
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作者：
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