Decreased expression of interleukin-37 and its anti-inflammatory effect in allergic rhinitis
Decreased expression of interleukin-37 and its anti-inflammatory effect in allergic rhinitis
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变应性鼻炎中白介素α37表达的降低及其抗炎作用
DOI：
10.3892/mmr.2017.7988
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发表时间：
2018-01-01
影响因子：
3.4
通讯作者：
Hong, Su-Ling
中科院分区：
文献类型：
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作者：
Shen, Yang;Ke, Xia;Hong, Su-Ling
白细胞介素-37（IL-37）是IL-1细胞因子家族的新成员，被认为是天然的天然免疫和炎症反应抑制因子。本研究旨在检测IL-37在变应性鼻炎（AR）患者外周血单个核细胞（PBMC）中的表达，探讨IL-37对炎症介质和CD 4 + T细胞的免疫抑制作用在AR发病机制中的作用。采用逆转录-定量聚合酶链反应（RT-qPCR）分析和流式细胞术测定39例AR患者和43例对照者PBMC中IL-37的表达水平。使用酶联免疫吸附试验和RT-qPCR分析，测定在存在或不存在IL-37的情况下用脂多糖刺激的PBMC和CD 4（+）T细胞上清液中的细胞因子。结果表明，AR患者PBMC中IL-37表达明显降低，IL-1和IL-6表达明显升高。重组IL-37（rIL-37）可抑制AR患者和正常人PBMC中IL-1 β和IL-6的产生，增强IL-27的产生。rIL-37还显著降低AR患者和对照组中CD 4（+）T细胞IL-17的表达。提示IL-37可能是AR发病机制中的重要细胞因子。它可能通过抑制促炎细胞因子的产生和通过抑制性调节Th 17应答而在AR中具有保护作用。
Interleukin-37 (IL-37), a novel member of the IL-1 cytokine family has been identified as a natural suppressor of innate immunity and inflammatory responses. The present study aimed to determine the expression of IL-37 in peripheral blood mononuclear cells (PBMCs) from patients with allergic rhinitis (AR), and examine the possible immunosuppressive effect of IL-37 on inflammatory mediators and CD4(+) T cells in the pathogenesis of AR. The expression levels of IL-37 were determined in PBMCs from 39 patients with AR and 43 controls using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) analysis and flow cytometry. Cytokines in the supernatants of the PBMCs and CD4(+) T cells, which were stimulated with lipopolysaccharide in the presence or absence of IL-37, were assayed using enzyme-linked immunosorbent assays and RT-qPCR analysis. The results showed that the patients with AR exhibited significantly decreased expression of IL-37, and increased expression levels of interleukin (IL)-1 and IL-6 in PBMCs. Recombinant IL-37 (rIL-37) inhibited the production of IL-1p and IL-6, and enhanced the production of IL-27 in PBMCs from the patients with AR and the control individuals. rIL-37 also markedly decreased the expression of IL-17 by CD4(+) T cells in the patients with AR and controls. These results suggested that IL-37 may be an important cytokine in the pathogenesis of AR. It may have a protective role in AR by inhibiting the production of proinflammatory cytokines and through suppressive regulation of the Th17 response.