Objective To analyze serum levels of interleukin-17(IL-17), interleukin-36 (IL-36) and eosinophil (EOS) count in children with bronchial asthma, and to discuss the clinical significance. Methods Totally 65 children with asthma were enrolled from July 2017 to July 2018 in Weifang People′s Hospital, of whom 30 cases were in acute exacerbation, 35 cases were in remission, and 25 health children were as control group. The serum levels of IL-17 and IL-36 were detected by enzyme-linked immunosorbent assay (ELISA), the eosinophil count in peripheral blood was measured by hematology analyzer, and the statistical analysis was performed. Results 1) The serum levels of IL-17 in acute exacerbation group[(45.73±8.86)pg/ml] and remission group[(21.06±5.51)pg/ml] were significantly higher than that in control group[(7.29±4.29)pg/ml] (P<0.01), and serum levels of IL-17 in acute exacerbation group was significantly higher than that in remission group(P<0.01). 2) The serum levels of IL-36 in acute exacerbation group[(53.76±10.60)pg/ml ] and remission group [(24.45±6.59) pg/ml] were significantly higher than that in control group[(8.46±4.86) pg/ml] (P<0.01), and serum level of IL-36 in acute exacerbation group was significantly higher than those in remission group(P<0.01). 3) In asthma children, serum level of IL-17 were positively correlated with the level of IL-36(P<0.01), and significant correlation were noted between the serum levels of IL-17, IL-36 and EOS count (P<0.01). Conclusion IL-17 and IL-36 are all involved in the pathogenesis of serum asthma in children, and serum levels of IL-17 and IL-36 may become a good biomarker for the diagnosis and evaluation of severity of asthma children.
Key words
bronchial asthma /
interleukin-17 /
interleukin-36 /
eosinophil /
children
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References
[1] 全国儿科哮喘协作组等. 第三次中国城市儿童哮喘流行病学调查[J]. 中华儿科杂志, 2013, 51(10): 729-735.
[2] Shin TS, Lee BJ, Tae YM, et al. Role of inducible nitric oxide synthase on the development of virus-associated asthma exacerbation which is dependent on Th1 and Th17 cell responses[J].Exp Mol Med,2010, 42(10): 721-730.
[3] Gresnlgt MS, van de Veerdon KFL. Biology of IL-36 cytokines and their role in disease[J]. Semin Immunol, 2013, 25(6): 458-465.
[4] 中华医学会儿科分会呼吸学组. 儿童支气管哮喘诊断与防治指南(2016年版)[J]. 中华儿科杂志, 2016, 54(3): 167-180.
[5] Pridgeon C, Bugeon L, Donnelly L, et al. Regulation of IL-17 in chronic inflammation in the human lung[J]. Clinical Science, 2011, 120(12): 515-524.
[6] Irvin C, Zafar I, Good J, et al. Increased frequency of dual-positive TH2/TH17 cells in bronchoalveolar lavage fluid characterizes a population of patients with severe asthma[J]. J Allergy Clin Immunol, 2014, 134(5): 1175-1186.
[7] Hallstrand TS, Lai Y, Altemeier WA, et al. Regulation and function of epithelial secreted phospholipase A2 group X in asthma[J]. Am J Respir Crit Care Med, 2013, 188(1): 42-50.
[8] 沈红燕, 杨丽萍, 杨芳. 支气管哮喘儿童血清IL-17、IL-35水平与肺功能的相关性分析[J].中国妇幼保健, 2017, 32(20): 5002-5004.
[9] Dietrich D, Martin P, Flacher V, et al. Interleukin-36 potently stimulates human M2 macrophages,langerhans cells and keratinocytes to produce pro-inflammatory cytokines[J]. Cytokine, 2016, 84: 88-98.
[10] Ramadas RA, Ewart SL, Medoff BD, et al. Interleukin-1 family member 9 stimulates chemokine production and neutrophil influx in mouse lungs[J]. Am J Resp Cell Mol, 2011, 44(2): 134-145.
[11] Ramadas RA, Ewart SL, Iwakura Y, et al. IL-36α exerts proinflammatory effects in the lungs of mice[J]. PLoS One, 2012, 7(9): e45784-e45784.
[12] 赵艳景,鲍文华,李树民,等. 支气管哮喘患者呼出气一氧化氮、血清IL-36水平及其相关性[J]. 临床肺科杂志, 2018, 23(2): 312-314.
[13] Dunn E, Sims JE, Nicklin MJH, et al. Annotating genes with potential roles in the immune system: six new members of the IL-1 family[J]. Trends Immunol, 2001, 22(10): 533-536.
[14] 王静静, 宋昕阳, 钱友存. 白介素-17家族细胞因子的研究进展[J]. 生命科学, 2016, 28(2): 170-181.