慢性阻塞性肺疾病患者血清IL-33及受体ST2水平的变化及分析
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摘要
目的探讨白细胞介素33(IL-33)及受体ST2在慢性阻塞性肺疾病发病机制中的作用。方法收集慢性阻塞性肺疾病(简称慢阻肺)患者50例及健康对照者30例,用ELISA法检测入组人群外周血中IL-33及其受体ST2的含量,并分析IL-33的表达水平与其受体ST2以及气流受限之间的相关性。结果慢阻肺患者外周血血清中IL-33[(311. 21±16. 21) pg/m L]及受体ST2的含量[(3. 069±0. 17) pg/m L]均明显高于健康对照者,差异有统计学意义(P <0. 05)。慢阻肺患者外周血血清中IL-33水平与其受体ST2含量呈正相关关系(r=0. 336,P=0. 02),与肺功能FEV_1/FVC呈负相关(r=-0. 455,P=0. 001)。结论 IL-33在慢阻肺发病过程中具有促进炎症反应的作用,此过程可能与其受体ST2有关。
Objective To investigate the possible roles of IL-33 and the receptor ST2 in chronic obstructive pulmonary disease( COPD). Methods 50 patients with COPD and 30 healthy subjects were recruited. The concentrations of IL-33 and ST2 in serum were measured by enzyme-linked immunosorbent assay( ELISA). The correlations among IL-33,ST2 and lung function test were performed. Results The serum level of IL-33 [( 311. 21 ± 16. 21)pg/m L]and ST2 [( 3. 069 ± 0. 17) ng/m L]was significantly higher in COPD patients than in healthy subjects( P <0. 05). Moreover,the serum IL-33 level in COPD was positively correlated with the serum ST2 level( r = 0. 336,P= 0. 02). The serum IL-33 level in COPD was negatively correlated with FEV_1/FVC( r =-0. 455,P = 0. 001).Conclusion IL-33 and ST2 may be involved in the pathogenesis of airway inflammation in COPD.
Objective To investigate the possible roles of IL-33 and the receptor ST2 in chronic obstructive pulmonary disease( COPD). Methods 50 patients with COPD and 30 healthy subjects were recruited. The concentrations of IL-33 and ST2 in serum were measured by enzyme-linked immunosorbent assay( ELISA). The correlations among IL-33,ST2 and lung function test were performed. Results The serum level of IL-33 [( 311. 21 ± 16. 21)pg/m L]and ST2 [( 3. 069 ± 0. 17) ng/m L]was significantly higher in COPD patients than in healthy subjects( P <0. 05). Moreover,the serum IL-33 level in COPD was positively correlated with the serum ST2 level( r = 0. 336,P= 0. 02). The serum IL-33 level in COPD was negatively correlated with FEV_1/FVC( r =-0. 455,P = 0. 001).Conclusion IL-33 and ST2 may be involved in the pathogenesis of airway inflammation in COPD.
引文
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[3] KAKKAR R,HEI H,DOBNER S,et al. Interleukin 33 as a mechanically responsive cytokine secreted by living cells[J]. J Biol Chem,2012,287(9):6941-6948.
[4] WU H,YANG S,WU X,et al. Interleukin-33/ST2 signaling promotes production of interleukin-6 and interleukin-8 in systemic inflammation in cigarette smoke-induced chronic obstructive pulmonary disease mice[J]. Biochem Biophys Res Commun,2014,450(1):110-116.
[5] BATEMAN E D,HURD S S,BARNES P J,et al. Global strategy for asthma management and prevention:GINA executive summary[J]. Eur Respir J,2008,31(1):143-178.
[6] KIM S W,RHEE C K,KIM K U,et al. Factors associated with plasma IL-33 levels in patients with chronic obstructive pulmonary disease[J]. Int J Chron Obstruct Pulmon Dis,2017,12:395-402.
[7] NG S C,ABU SAMAH F,HELMY K,et al. Comparison between FEV1/FEV6 and FEV1/FVC as screening of chronic obstructive pulmonary disease[J]. Med J Malaysia,2017,72(5):286-290.