张凌伟,锁海虹,苏学艳,刘冬莲,王桂荣,李 芳.特应性皮炎患儿外周血miR-122a和miR-146a水平与Th1/Th2/Th17免疫平衡的相关性分析[J].,2024,(9):1751-1755 |
特应性皮炎患儿外周血miR-122a和miR-146a水平与Th1/Th2/Th17免疫平衡的相关性分析 |
Correlation Analysis of Peripheral Blood miR-122a and miR-146a Levels and Th1/Th2/Th17 Immune Balance in Children with Atopic Dermatitis |
投稿时间:2023-11-11 修订日期:2023-11-30 |
DOI:10.13241/j.cnki.pmb.2024.09.030 |
中文关键词: 特应性皮炎 miR-122a miR-146a Th1/Th2/Th17免疫平衡 相关性 |
英文关键词: Atopic dermatitis miR-122a miR-146a Th1/Th2/Th17 immune balance Correlation |
基金项目:河北省中医药管理局2020年度中医药类科研计划课题(2020289) |
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中文摘要: |
摘要 目的:探讨特应性皮炎(AD)患儿外周血微小核糖核酸(miRNA)-122a和miR-146a水平与辅助性T细胞(Th)1/Th2/Th17免疫平衡的相关性。方法:选取2020年5月~2023年5月石家庄市妇幼保健院皮肤科收治的AD患儿100例为AD组,根据特应性皮炎评分(SCORAD)分为轻度组31例、中度组41例、重度组28例,另选取同期100名体检健康儿童为对照组。采用实时荧光定量聚合酶链式反应检测外周血miR-122a、miR-146a水平,流式细胞术检测外周血Th1、Th2、Th17细胞比例,酶联免疫吸附法检测外周血Th1、Th2、Th17相关细胞因子[白细胞介素(IL)-2、干扰素-γ(IFN-γ)、IL-4、IL-13、IL-17、IL-22]水平,并计算Th1/Th2/Th17比值。采用Pearson/Spearman相关性分析AD患儿外周血miR-122a、miR-146a与Th1、Th2、Th17和相关细胞因子及Th1/Th2/Th17的相关性。结果:AD组外周血miR-122a、miR-146a、Th1、Th1/Th2/Th17、IL-2、IFN-γ水平低于对照组,Th2、Th17、IL-4、IL-13、IL-17、IL-22水平高于对照组(P均<0.05)。轻度组、中度组、重度组外周血miR-122a、miR-146a、Th1、Th1/Th2/Th17、IL-2、IFN-γ水平依次降低,Th2、Th17、IL-4、IL-13、IL-17、IL-22水平依次升高(P均<0.05)。Pearson/Spearman相关性分析显示,AD患儿外周血miR-122a、miR-146a与Th1、Th1/Th2/Th17、IL-2、IFN-γ水平呈正相关(r/rs分别为0.679、0.677、0.684、0.706、0.693、0.689、0.671、0.694,P均<0.001),与Th2、Th17、IL-4、IL-13、IL-17、IL-22呈负相关(r/rs分别为-0.690、-0.680、-0.681、-0.669、-0.675、-0.676、-0.676、-0.686、-0.682、-0.674、-0.680、-0.689,P均<0.001)。结论:AD患儿外周血miR-122a、miR-146a水平降低,与病情严重程度密切相关,可能通过调节Th1/Th2/Th17免疫平衡参与AD发生发展。 |
英文摘要: |
ABSTRACT Objective: To investigate the correlation between peripheral blood microRNA (miRNA)-122a and miR-146a levels and T helper cells (Th)1/Th2/Th17 immune balance in children with atopic dermatitis (AD). Methods: 100 children with AD who were admitted to the Dermatology Department of Shijiazhuang Maternal and Child Health Hospital from May 2020 to May 2023 were selected as AD group. According to scoring atopic dermatitis (SCORAD), they were divided into mild group with 31 cases, moderate group with 41 cases and severe group with 28 cases. Another 100 healthy children during the same period were selected as control group. Real-time fluorescence quantitative polymerase chain reaction was used to detect the levels of peripheral blood miR-122a and miR-146a, and flow cytometry was used to detect the proportion of peripheral blood Th1, Th2 and Th17 cells. The levels of peripheral blood Th1, Th2 and Th17-related cytokines [interleukin (IL) -2, interferon-γ (IFN-γ), IL-4, IL-13, IL-17, IL-22] were detected by enzyme-linked immunosorbent assay, and the ratio of Th1/Th2/Th17 was calculated. The correlations of peripheral blood miR-122a, miR-146a and Th1, Th2, Th17 and related cytokines and Th1/Th2/Th17 of children with AD were analyzed by Pearson/Spearman correlation analysis. Results: The levels of peripheral blood miR-122a, miR-146a, Th1, Th1/Th2/Th17, IL-2 and IFN-γ of the AD group were lower than those of the control group, and the levels of Th2, Th17, IL-4, IL-13, IL-17 and IL-22 were higher than those of the control group (all P<0.05). The levels of peripheral blood miR-122a, miR-146a, Th1, Th1/Th2/Th17, IL-2 and IFN-γ of the mild group, moderate group and severe group were decreased successively, while the levels of Th2, Th17, IL-4, IL-13, IL-17 and IL-22 were increased successively (all P<0.05). Pearson/Spearman correlation analysis showed that peripheral blood miR-122a and miR-146a in children with AD were positively correlated with the levels of Th1, Th1/Th2/Th17, IL-2, and IFN-γ (r/rs were 0.679, 0.677, 0.684, 0.706, 0.693, 0.689, 0.671, 0.694, respectively, all P<0.001), and negatively correlated with Th2, Th17, IL-4, IL-13, IL-17, IL-22 (r/rs were -0.690, -0.680, -0.681, -0.669, -0.675, -0.676, -0.676, -0.686, -0.682, -0.674, -0.680, -0.689, respectively, all P<0.001). Conclusion: The decreased levels of peripheral blood miR-122a and miR-146a of patients with AD are closely related to the severity of the disease, and which may participate in the occurrence and development of AD by regulating the Th1/Th2/Th17 immune balance. |
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