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和基因的遗传多态性对牙周炎免疫发病机制的影响。

The Influence of Genetic Polymorphisms of and Genes on the Immunopathogenesis of Periodontitis.

作者信息

Yamanaka Aléia Harumi Uchibaba, de Alencar Josiane Bazzo, de Souza Victor Hugo, Zacarias Joana Maiara Valentini, Bahls-Pinto Larissa Danielle, Silva Cléverson O, Sell Ana Maria, de Lima Neto Quirino Alves

机构信息

Department of Clinical Analysis and Biomedicine, Maringá State University, Maringá, Paraná, Brazil.

Department of Basic Chairs, Marília Medical School-FAMEMA, Marília, São Paulo, Brazil.

出版信息

Int J Dent. 2025 May 2;2025:7599713. doi: 10.1155/ijod/7599713. eCollection 2025.

DOI:10.1155/ijod/7599713
PMID:40352809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12064316/
Abstract

Periodontitis (PD) is an inflammatory disease that affects the protective and supporting tissues of teeth. Mutations in cytokines and their receptors may influence the immunopathogenesis of PD, but the role of interleukin-33 (IL-33) and IL1RL1 is not clear. Thus, this study aimed to analyze the polymorphisms in (rs1929992 and rs7025417) and (rs11685424 and rs3821204) genes and the IL-33 serum levels in PD patients. A case-control study was performed with 186 PD patients and 189 controls. Genotyping was performed by polymerase chain reaction using sequence-specific primer (PCR-SSP) technique. Serum levels of IL-33 were determined using the immunoenzymatic method. Statistical analyses were performed using SNPStats and OpenEpi. > 0.05 was considered statistically significant. The rs7025417 C/C genotype was a risk factor for PD in nonsmokers (=0.0015) regardless of smoking status and gender. In the general population, the rs3821204 G/G genotype was protective for PD (=0.006), regardless of gender. Nevertheless, the IL-33 serum levels were increased in patients compared to controls ( < 0.0001); however, no difference was observed among PD patients. The polymorphisms rs7025417 and rs3821204 were associated with risk and protection, respectively, and the production of IL-33 was higher in PD patients than in controls, independent of the extent or severity of the disease.

摘要

牙周炎(PD)是一种影响牙齿保护和支持组织的炎症性疾病。细胞因子及其受体的突变可能会影响牙周炎的免疫发病机制,但白细胞介素-33(IL-33)和IL1RL1的作用尚不清楚。因此,本研究旨在分析IL1RL1基因(rs1929992和rs7025417)和IL33基因(rs11685424和rs3821204)的多态性以及牙周炎患者的IL-33血清水平。对186例牙周炎患者和189例对照进行了病例对照研究。采用序列特异性引物聚合酶链反应(PCR-SSP)技术进行基因分型。使用免疫酶法测定IL-33的血清水平。使用SNPStats和OpenEpi进行统计分析。P>0.05被认为具有统计学意义。无论吸烟状况和性别如何,IL1RL1基因的rs7025417 C/C基因型是非吸烟者患牙周炎的危险因素(P=0.0015)。在普通人群中,无论性别如何,IL33基因的rs3821204 G/G基因型对牙周炎具有保护作用(P=0.006)。然而,与对照组相比,患者的IL-33血清水平升高(P<0.0001);然而,在牙周炎患者中未观察到差异。IL1RL1基因的rs7025417和IL33基因的rs3821204多态性分别与风险和保护相关,并且牙周炎患者中IL-33的产生高于对照组,与疾病的范围或严重程度无关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b59/12064316/a04b17eba6b5/IJD2025-7599713.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b59/12064316/a04b17eba6b5/IJD2025-7599713.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b59/12064316/a04b17eba6b5/IJD2025-7599713.001.jpg

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本文引用的文献

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PLoS One. 2023 Mar 22;18(3):e0283179. doi: 10.1371/journal.pone.0283179. eCollection 2023.
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Role of the IL33 and IL1RL1 pathway in the pathogenesis of Immunoglobulin A vasculitis.IL33 和 IL1RL1 通路在免疫球蛋白 A 血管炎发病机制中的作用。
Sci Rep. 2021 Aug 9;11(1):16163. doi: 10.1038/s41598-021-95762-5.
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, , and Gene Polymorphisms on Hepatocellular Carcinoma Susceptibility in the Chinese Population.基因多态性与中国人群肝癌易感性的关系。
Biomed Res Int. 2020 Sep 29;2020:2918517. doi: 10.1155/2020/2918517. eCollection 2020.
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The Influence of , , , and Polymorphisms in Periodontitis: A Case-Control Study.牙周炎中 、 、 、 多态性的影响:一项病例对照研究。
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