β 2糖蛋白I对放线菌聚集菌的分子模拟。

D Wang, T Nagasawa, Y Chen, Y Ushida, H Kobayashi, Y Takeuchi, M Umeda, Y Izumi
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引用次数: 28

摘要

简介:β -糖蛋白I (beta 2GPI)在抑制凝血中起重要作用,β 2GPI分子上抗TLRVYK肽的抗体与血栓形成有关。根据Swiss-Prot数据库,Aggregatibacter actiomycetemcomitans leukotoxin c具有与TLRVYK肽同源的序列(SIRVYK)。本研究旨在探讨放线菌感染对牙周炎患者抗SIRVYK肽抗体反应的影响。方法:采用酶联免疫吸附法测定46例侵袭性牙周炎患者(局限性8例,全身性38例)、28例慢性牙周炎患者和20例牙周健康者血清抗SIRVYK或TLRVYK肽的免疫球蛋白G (IgG)抗体和IgG亚类抗体滴度。采用聚合酶链反应测定菌斑和唾液样本中放线菌的存在。结果:慢性牙周炎组放线菌A.阳性患者抗sirvyk抗体水平明显高于放线菌A.阴性患者(P < 0.05)。抗体对TLRVYK肽的反应也有类似的趋势;然而,放线菌杆菌阳性和阴性患者之间无统计学差异。A.放线菌comitans阳性患者抗sirvyk IgG2和IgG3抗体水平显著高于A.放线菌comitans阴性患者(P < 0.05)。IgG2水平在4个IgG亚类中最高,且主要在放线菌单胞杆菌阳性患者中升高。抗tlrvyk抗体水平与抗sirvyk IgG抗体水平显著相关。结论:放线菌感染可引起牙周炎患者抗sirvyk IgG抗体,并通过β 2gpi分子模拟改变抗tlrvyk抗体反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular mimicry of Aggregatibacter actinomycetemcomitans with beta2 glycoprotein I.

Introduction: beta2-Glycoprotein I (beta 2GPI) is important in the suppression of coagulation, and antibodies against TLRVYK peptides on the beta 2GPI molecule are related to thrombosis. According to the Swiss-Prot database, Aggregatibacter actinomycetemcomitans leukotoxin c has sequences (SIRVYK) that are homologous to the TLRVYK peptides. The aim of this study was to investigate the effects of A. actinomycetemcomitans infection on the antibody response against SIRVYK peptides in patients with periodontitis.

Methods: Serum immunoglobulin G (IgG) antibody and IgG subclass antibody titers against SIRVYK or TLRVYK peptides were measured by enzyme-linked immunosorbent assay in 46 patients with aggressive periodontitis (eight with localized disease, 38 with generalized disease), 28 patients with chronic periodontitis, and 20 periodontally healthy subjects. The presence of A. actinomycetemcomitans in plaque and saliva samples was determined using polymerase chain reaction.

Results: The level of anti-SIRVYK antibodies was significantly higher in patients who were A. actinomycetemcomitans-positive than in A. actinomycetemcomitans-negative patients (P < 0.05) in the chronic periodontitis group. A similar trend was found in the antibody response to TLRVYK peptide; however, no statistically significant difference was seen between A. actinomycetemcomitans-positive and -negative patients. The A. actinomycetemcomitans-positive patients displayed significantly higher levels of anti-SIRVYK IgG2 and IgG3 antibodies than A. actinomycetemcomitans-negative patients (P < 0.05 and P < 0.05, respectively). The level of IgG2 was highest among the four IgG subclasses and it predominantly increased in patients who were A. actinomycetemcomitans-positive. Anti-TLRVYK antibody levels were significantly correlated with anti-SIRVYK IgG antibody levels.

Conclusion: The results suggest that A. actinomycetemcomitans infection may elicit anti-SIRVYK IgG antibodies and modify the anti-TLRVYK antibody response in patients with periodontitis by molecular mimicry with beta2GPI.

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