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白细胞介素17A和17B在牙周炎患者牙龈组织中的表达

Expression of Interleukin 17A and 17B in Gingival Tissue in Patients with Periodontitis.

作者信息

Mazurek-Mochol Małgorzata, Serwin Karol, Bonsmann Tobias, Kozak Małgorzata, Piotrowska Katarzyna, Czerewaty Michał, Safranow Krzysztof, Pawlik Andrzej

机构信息

Department of Periodontology, Pomeranian Medical University, 70-111 Szczecin, Poland.

Department of Physiology, Pomeranian Medical University, 70-111 Szczecin, Poland.

出版信息

J Clin Med. 2023 Jul 11;12(14):4614. doi: 10.3390/jcm12144614.

DOI:10.3390/jcm12144614
PMID:37510729
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10380614/
Abstract

Periodontitis (PD) is a chronic inflammatory disease that is initiated by oral microorganisms. The pathogens induce the production of cytokines, such as interleukin (IL)-17, which enhances the inflammatory response and progression of the disease. The aim of this study was to examine the expression and localization in gingival tissue of IL-17A and IL-17B in patients with periodontitis. This study included 14 patients with periodontal disease and 14 healthy subjects without periodontal disease as a control group. There were no statistically significant differences in the expression of mRNA between patients with periodontitis and control subjects. The expression of mRNA was statistically significantly lower in patients with periodontitis in comparison with healthy subjects ( < 0.048). The expression of correlated significantly with the approximal plaque index. The expression in gingival tissue correlated with the clinical attachment level. This correlation reached borderline statistical significance ( = 0.06). In immunohistochemical analysis, we have shown the highest expression of IL-17 protein in inflamed connective tissue, epithelium, and granulation tissue from gingival biopsy specimens from patients with periodontitis. In biopsy specimens from healthy individuals, no IL-17 was found in the epithelium, while an expression of IL-17 was found in the connective tissue. The results of our study confirm the involvement of IL-17 in the pathogenesis of periodontitis. Our results suggest that an increase in IL-17 protein expression in the gingival tissue of patients with periodontitis occurs at the post-translational stage.

摘要

牙周炎(PD)是一种由口腔微生物引发的慢性炎症性疾病。这些病原体诱导细胞因子的产生,如白细胞介素(IL)-17,其会增强炎症反应以及疾病的进展。本研究的目的是检测牙周炎患者牙龈组织中IL-17A和IL-17B的表达及定位。本研究纳入了14例牙周疾病患者和14名无牙周疾病的健康受试者作为对照组。牙周炎患者与对照组受试者之间mRNA表达无统计学显著差异。与健康受试者相比,牙周炎患者的mRNA表达在统计学上显著更低(<0.048)。的表达与邻面菌斑指数显著相关。牙龈组织中的表达与临床附着水平相关。这种相关性达到了临界统计学显著性(=0.06)。在免疫组织化学分析中,我们发现牙周炎患者牙龈活检标本的炎症结缔组织、上皮和肉芽组织中IL-17蛋白表达最高。在健康个体的活检标本中,上皮中未发现IL-17,而在结缔组织中发现了IL-17的表达。我们的研究结果证实了IL-17参与牙周炎的发病机制。我们的结果表明,牙周炎患者牙龈组织中IL-17蛋白表达的增加发生在翻译后阶段。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/e6ab764a2b27/jcm-12-04614-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/271fab195dd3/jcm-12-04614-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/a50a0066d2ff/jcm-12-04614-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/e6ab764a2b27/jcm-12-04614-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/271fab195dd3/jcm-12-04614-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/a50a0066d2ff/jcm-12-04614-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6bc/10380614/e6ab764a2b27/jcm-12-04614-g003.jpg

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本文引用的文献

1
Periodontal diagnosis in the context of the 2017 classification system of periodontal diseases and conditions - implementation in clinical practice.牙周病分类系统(2017 版)下的牙周病诊断——临床实践中的应用。
Br Dent J. 2019 Jan 11;226(1):16-22. doi: 10.1038/sj.bdj.2019.3.
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Periodontitis: Consensus report of workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.牙周炎:2017 年牙周病和种植体周围疾病分类世界研讨会工作组 2 的共识报告。
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Salivary Concentrations of Interleukin (IL)-1β, IL-17A, and IL-23 Vary in Relation to Periodontal Status.
白细胞介素(IL)-1β、IL-17A和IL-23的唾液浓度随牙周状况而变化。
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Periodontitis-associated pathogens P. gingivalis and A. actinomycetemcomitans activate human CD14(+) monocytes leading to enhanced Th17/IL-17 responses.与牙周炎相关的病原体牙龈卟啉单胞菌和伴放线放线杆菌激活人CD14(+)单核细胞,导致Th17/白细胞介素-17反应增强。
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