Charrad Rihab, Berraïes Anissa, Hamdi Besma, Ammar Jamel, Hamzaoui Kamel, Hamzaoui Agnes
Unit Research 12SP15 "Homeostasis and Cell Dysfunction", Abderrahman Mami Hospital, Ariana,Tunisia; El Manar Tunis University, Faculty of Medicine of Tunis, Department of Basic Sciences, Tunis, Tunisia.
Unit Research 12SP15 "Homeostasis and Cell Dysfunction", Abderrahman Mami Hospital, Ariana,Tunisia; El Manar Tunis University, Faculty of Medicine of Tunis, Department of Basic Sciences, Tunis, Tunisia; Division of Pulmonology, Department of Paediatric Respiratory Diseases, Abderrahman Mami Hospital, Ariana, Tunisia.
Immunobiology. 2016 Feb;221(2):182-7. doi: 10.1016/j.imbio.2015.09.009. Epub 2015 Sep 8.
The aim of this study was to assess interleukin (IL)-37 production in asthmatic children in serum and induced sputum and to look to the impact of IL-37 on pro-inflammatory cytokines production (TNF-α, IL-6, IL-1β and IL-17).
Forty children with well-controlled asthma (20 moderate and 20 mild asthmatics) were studied. IL-37 was measured by ELISA in serum and induced sputum (IS) samples, and compared with 22 age- and sex-matched healthy controls. Real-time quantitative PCR was used to determine IL-37 mRNA expression in induced sputum cells. Induced sputum mononuclear cells from 10 moderate asthmatics and 10 healthy controls were stimulated either with lipopolysaccharides (LPS) or LPS plus recombinant IL-37 (rIL-37) comparing pro-inflammatory cytokines production. TNF-α, IL-1β, IL-6 and IL-17 were measured by RT-PCR and ELISA.
The expression of IL-37 mRNA in asthmatic patients was significantly lower than that observed in healthy controls (P=0.0001). IL37 mRNA expression depended on asthma severity. Serum and IS IL-37 levels were significantly lower in asthma patients compared to healthy controls. LPS-stimulated sputum cells from asthma patients produced higher levels of IL-1β, IL-6, and TNF-α than those from HC. Adding rIL-37 suppressed TNF-α, IL-1β and IL-6 production in IS cells. In the same way, stimulating IS CD4(+) T cells in the presence of rIL-37 inhibited IL-17 production both in asthma patients and HC. IL-37 effect on IL-17 was more pronounced in patients than controls.
The decrease in IL-37 level observed in IS was found to correlate with disease severity. The increased pro-inflammatory cytokines production from asthma IS cells was abrogated by the addition of rIL-37. IL-37 could be an important cytokine in the control of asthma by suppressing the production of inflammatory cytokines.
本研究旨在评估哮喘儿童血清和诱导痰中白细胞介素（IL）-37的产生情况，并观察IL-37对促炎细胞因子（肿瘤坏死因子-α、IL-6、IL-1β和IL-17）产生的影响。
对40例病情得到良好控制的哮喘儿童（20例中度哮喘患者和20例轻度哮喘患者）进行研究。采用酶联免疫吸附测定法（ELISA）检测血清和诱导痰样本中的IL-37，并与22例年龄和性别匹配的健康对照者进行比较。采用实时定量聚合酶链反应（PCR）测定诱导痰细胞中IL-37 mRNA的表达。用脂多糖（LPS）或LPS加重组IL-37（rIL-37）刺激10例中度哮喘患者和10例健康对照者的诱导痰单核细胞，比较促炎细胞因子的产生情况。采用逆转录PCR（RT-PCR）和ELISA检测肿瘤坏死因子-α、IL-1β、IL-6和IL-17。
哮喘患者中IL-37 mRNA的表达明显低于健康对照者（P = 0.0001）。IL-37 mRNA的表达取决于哮喘的严重程度。与健康对照者相比，哮喘患者血清和诱导痰中的IL-37水平明显较低。LPS刺激的哮喘患者痰细胞产生的IL-1β、IL-6和肿瘤坏死因子-α水平高于健康对照者。添加rIL-37可抑制诱导痰细胞中肿瘤坏死因子-α、IL-1β和IL-6的产生。同样，在rIL-37存在的情况下刺激诱导痰CD4(+) T细胞可抑制哮喘患者和健康对照者中IL-17的产生。IL-37对IL-17的作用在患者中比在对照者中更明显。
发现诱导痰中观察到的IL-37水平降低与疾病严重程度相关。添加rIL-37可消除哮喘诱导痰细胞中促炎细胞因子产生的增加。IL-37可能是通过抑制炎性细胞因子的产生来控制哮喘的一种重要细胞因子。
Zotero 插件