慢性阻塞性肺病患者血清IL-21、IL-6、IL-17的水平及意义
发布时间：2018-09-17 18:36
【摘要】：目的:通过检测对比慢性阻塞性肺病急性加重期与稳定期患者、健康患者血清IL-21、IL-17、IL-6、RORγt的表达并分析其与疾病严重程度及临床相关指标的关系,进一步研究IL-21-RORγt-IL-21、IL-17炎症反应轴、IL-6/IL-21-肺动脉轴与慢性阻塞性肺病的炎症反应、肺气肿、肺血管病变的关系,为慢性阻塞性肺病的研究提供新的理论基础和方向。方法:选取2015年9月-2016年9月到青岛大学附属医院呼吸内科就诊的COPD的患者120例,其中急性加重期患者60例作为急性期组,稳定期患者60例作为稳定期组;同期健康查体的患者60例作为健康对照组。所有患者均晨起抽取空腹静脉血,用酶联免疫法测定血清IL-21、IL-17、IL-6、RORγt的含量,并测定患者FEV1、FVC、FEV1/FVC、肺动脉内径、肺动脉压力、右心室的内径等指标。探讨三组数据之间上述指标的差异,用spss22进行统计学分析。结果:1.IL-21、IL-17、IL-6、RORγt血清IL-21的含量在急性加重期组为279.107±17.836 pg/ml,稳定期组为224.109±30.051 pg/ml,对照组为170.201±25.197 pg/ml,急性加重组高于稳定期组及健康对照组(t=11.8、26.63,P0.05),稳定期组表达显著高于健康对照组(t=10.34,P0.05)。血清IL-17的含量在急性加重期组为145.114±19.961 pg/ml,稳定期组为49.830±7.735 pg/ml,对照组为25.819±4.376 pg/ml,急性期组显著高于稳定期组、健康对照组(t=33.34、44.07,P0.05),稳定期组显著高于对照组(t=20.35,P0.001)。血清IL-6的含量在急性加重期组为39.414±3.225 pg/ml,稳定期组为32.598±3.475pg/ml,对照组为24.831±2.121 pg/ml,急性期组显著高于稳定期组、健康对照组(t=10.81、28.52,P0.05),稳定期组高于对照组(t=14.31,P0.05)。各组血清RORγt的含量在急性加重期组3.206±0.263 ng/ml,稳定期组为2.527±0.469ng/ml,对照组为2.095±0.271 ng/ml,急性期组显著高于稳定期组(t=8.33、18.4,P0.05)。稳定期组显著高于对照组(t=2.69,P0.05)。2.三组呼吸功能的检测在FEV1、FEV1/FVC方面,急性加重期低于稳定期组及健康对照组,稳定期低于健康对照组,三组差异具有统计学意义(P0.05)。在FVC方面,急性加重期FVC较健康对照组略有下降(P0.05)。3.血清C-反应蛋白、血沉、D-二聚体的表达在血清C-反应蛋白方面,急性加重期与稳定期及健康对照组相比存在显著差异,稳定期高于健康对照组,三组差异具有统计学意义(P0.05)。血沉在三组数据之间未见明显差异。急性加重期D-二聚体高于稳定期及正常期,差异有统计学意义(P0.05)。4.肺动脉内径、肺动脉压力、右心室内径肺动脉内径的测定结果为,急性加重期27.05±2.708 mm,稳定期24.98±1.833 mm,健康对照组23.77±1.851 mm,急性加重期与稳定期及健康对照组相比存在显著统计学差异(P0.05),稳定期的肺动脉内径高于健康对照组(P0.05)。肺动脉压力的测定结果为,急性加重期52.64±9.064 mm Hg,稳定期42.82±7.510 mm Hg,健康对照组28.85±2.641 mm Hg,急性加重期与稳定期及健康对照组相比存在显著差异(P0.05),稳定期的肺动脉压力高于健康对照组(P0.05)。右心室内径测定结果为,急性加重期28.42±3.731mm,稳定期26.41±3.218mm,健康对照组25.91±3.878mm,急性加重期高于健康对照组,存在显著统计学差异(P0.05)。稳定期高于正常期(P0.05)。5.COPD合并肺动脉高压组、COPD不合并合并肺动脉高压组与健康对照组之间IL-21的表达IL-21测定结果为,急性加重期273.26±23.45 pg/ml,稳定期230.88±39.02 pg/ml,健康对照组170.84±25.34 pg/ml。IL-6测定结果为,急性加重期为37.32±4.76pg/ml,稳定期为34.48±4.79 pg/ml,健康对照组为24.73±2.13 pg/ml,IL-21与IL-6在急性加重期均显著高于稳定期及健康对照组,稳定期的表达高于健康对照组(P0.05)。肺动脉压力的测定结果,急性加重期为56.23±6.89 mm,稳定期40.31±5.30 mm,健康对照组28.81±2.59 mm。肺动脉平均内径的测定结果为,急性加重期26.61±2.59 mm,稳定期25.51±2.34 mm,健康对照组23.72±1.89 mm,急性加重期与稳定期及健康对照组存在显著差异,稳定期高于健康对照组,数值具有统计学差异(P0.05)。6.相关分析血清IL-21与IL-17、IL-6、RORγt呈显著正相关(r=0.795、0.775、0.686,P0.05),与CRP呈显著正相关(r=0.611,P0.05);与FEV1/FVC、FEV1呈负相关(r=-0.729、-0.830,P0.05);与肺动脉平均内径、肺动脉压力呈显著正相关(r=0.448、0.802,P0.05)。结论:1.慢性阻塞性肺病患者血清IL-21表达明显增高,在COPD急性加重期更加显著,且IL-6、IL-17、RORγt呈显著正相关,提示IL-21参与到COPD的气道炎症过程中。IL-21可能通过IL-21-RORγt(TH17)-IL-17轴在慢性阻塞性肺病疾病进展过程中发挥重要作用,说明IL-21参与了COPD的炎症反应过程,并且起到一定的促炎作用,起到桥梁的作用。2.IL-21与气流受限指标FEV1/FVC呈显著负相关,与疾病严重程度指标FEV1呈负相关,提示IL-21参与了气流受限的过程,随着IL-21的表达量增加,疾病逐渐加重。3.COPD伴或不伴肺动脉高压与健康对照组IL-21、IL-6表达存在显著差异,且IL-21与IL-6、肺动脉平均内径、肺动脉压力呈显著正相关,提示IL-21通过IL-6/IL-21-肺血管途径参与了肺动脉血管改变、肺动脉高压形成的过程。
[Abstract]:Objective: To investigate the expression of IL-21, IL-17, IL-6 and ROR-gamma t in serum of patients with chronic obstructive pulmonary disease (COPD) at acute exacerbation stage and stable stage, and the relationship between IL-21-ROR-gamma t-IL-21, IL-17 inflammatory response axis, IL-6/IL-21 pulmonary artery axis and COPD. Methods: From September 2015 to September 2016, 120 patients with COPD were selected from the Department of Respiratory Medicine, Qingdao University Affiliated Hospital. Among them, 60 patients in acute exacerbation stage were treated as acute stage group and 60 patients in stable stage were treated as stable stage. All the patients got up in the morning and measured the levels of IL-21, IL-17, IL-6 and ROR gamma t by ELISA. The indexes of FEV1, FVC, FEV1/FVC, pulmonary artery diameter, pulmonary artery pressure and right ventricular diameter were also measured. Results: 1. The serum levels of IL-21, IL-17, IL-6 and ROR gamma t in the acute exacerbation group were 279.107 (+ 17.836) pg/ml, 224.109 (+ 30.051) pg/ml in the stable phase group and 170.201 (+ 25.197) pg/ml in the control group. The levels of IL-21, IL-17, IL-6 and ROR gamma t in the acute exacerbation group were higher than those in the stable phase group and the healthy control group (t = 11.8, 26.63, P 0.05). The level of serum IL-17 in acute exacerbation group was 145.114 (+19.961) pg/ml, stable phase group was 49.830 (+7.735) pg/ml, control group was 25.819 (+4.376) pg/ml, acute phase group was significantly higher than stable phase group, healthy control group (t = 33.34, 44.07, P 0.05), stable phase group was significantly higher than control group (t = 20.35, P 0.0.05). The serum levels of IL-6 in acute exacerbation group were 39.414+3.225 pg/ml, 32.598+3.475 pg/ml in stable phase group, 24.831+2.121 pg/ml in control group, significantly higher in acute phase group than in stable phase group, healthy control group (t = 10.81, 28.52, P 0.05), stable phase group was higher than that in control group (t = 14.31, P 0.05). 206 + 0.263 ng / ml, 2.527 + 0.469 ng / ml in stable phase group, 2.095 + 0.271 ng / ml in control group, significantly higher in acute phase group than in stable phase group (t = 8.33, 18.4, P 0.05). Respiratory function of stable phase group was significantly higher than that of control group (t = 2.69, P 0.05). 2. Respiratory function of three groups in FEV1, FEV1 / FVC was lower in acute exacerbation phase than that of stable phase group and healthy control group. The levels of serum C-reactive protein, erythrocyte sedimentation rate and D-dimer in acute exacerbation were significantly higher than those in stable and healthy control groups (P 0.05). There was no significant difference in ESR among the three groups. D-dimer in acute exacerbation was higher than that in stable and normal period. The difference was statistically significant (P 0.05). 4. The pulmonary artery diameter in the stable phase was higher than that in the healthy control group (P 0.05). The pulmonary artery pressure in the stable phase was higher than that in the stable phase (P 0.05). The pulmonary artery pressure in the stable phase was higher than that in the healthy control group (P Stable phase was higher than normal phase (P 0.05). 5. The expression of IL-21 in COPD patients with pulmonary hypertension and COPD patients without pulmonary hypertension was 273.26 (+ 23.45) pg/ml in acute exacerbation, 230.88 (+ 39.02) pg/ml in stable phase and 170.2 pg/ml in healthy control group. The results of IL-6 assay showed that the acute exacerbation stage was 37.32+4.76pg/ml, the stable stage was 34.48+4.79 pg/ml, the healthy control group was 24.73+2.13 pg/ml, the expressions of IL-21 and IL-6 in the acute exacerbation stage were significantly higher than those in the stable stage and healthy control group, and the expression of IL-6 in the stable stage was higher than that in the healthy control group (P 0.05). The mean internal diameter of pulmonary artery in the acute exacerbation stage was 26.61 (+ 2.59 mm), the stable stage was 25.51 (+ 2.34 mm) and the healthy control group was 23.72 (+ 1.89 mm). There were significant differences between the acute exacerbation stage and the stable stage and the healthy control group. Correlation analysis showed that serum IL-21 was positively correlated with IL-17, IL-6 and ROR gamma t (r = 0.795, 0.775, 0.686, P 0.05), and positively correlated with CRP (r = 0.611, P 0.05); negatively correlated with FEV1 / FVC, FEV1 (r = - 0.729, - 0.830, P 0.05); positively correlated with mean diameter of pulmonary artery and pulmonary artery pressure (r = 0.448, 0.802, P 0.05). Conclusion: 1. The expression of serum IL-21 in COPD patients was significantly increased, especially in acute exacerbation of COPD. IL-6, IL-17 and ROR-gamma T were positively correlated, suggesting that IL-21 was involved in the airway inflammation of COPD. IL-21 may play an important role in the progression of COPD through the IL-21-ROR-gamma t (TH17) -IL-17 axis. Interleukin-21 participated in the inflammatory process of COPD and played a role in promoting inflammation and bridging. 2. IL-21 was negatively correlated with airflow limitation index FEV1 / FVC, and negatively correlated with disease severity index FEV1, suggesting that IL-21 participated in the process of airflow limitation, with the increase of IL-21 expression, the disease gradually aggravated.3. COPD. The expression of IL-21 and IL-6 was significantly correlated with IL-6, mean pulmonary artery diameter and pulmonary artery pressure, suggesting that IL-21 participated in the process of pulmonary artery changes and pulmonary hypertension formation through the IL-6/IL-21 pulmonary vascular pathway.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R563.9
本文编号：2246766
[Abstract]:Objective: To investigate the expression of IL-21, IL-17, IL-6 and ROR-gamma t in serum of patients with chronic obstructive pulmonary disease (COPD) at acute exacerbation stage and stable stage, and the relationship between IL-21-ROR-gamma t-IL-21, IL-17 inflammatory response axis, IL-6/IL-21 pulmonary artery axis and COPD. Methods: From September 2015 to September 2016, 120 patients with COPD were selected from the Department of Respiratory Medicine, Qingdao University Affiliated Hospital. Among them, 60 patients in acute exacerbation stage were treated as acute stage group and 60 patients in stable stage were treated as stable stage. All the patients got up in the morning and measured the levels of IL-21, IL-17, IL-6 and ROR gamma t by ELISA. The indexes of FEV1, FVC, FEV1/FVC, pulmonary artery diameter, pulmonary artery pressure and right ventricular diameter were also measured. Results: 1. The serum levels of IL-21, IL-17, IL-6 and ROR gamma t in the acute exacerbation group were 279.107 (+ 17.836) pg/ml, 224.109 (+ 30.051) pg/ml in the stable phase group and 170.201 (+ 25.197) pg/ml in the control group. The levels of IL-21, IL-17, IL-6 and ROR gamma t in the acute exacerbation group were higher than those in the stable phase group and the healthy control group (t = 11.8, 26.63, P 0.05). The level of serum IL-17 in acute exacerbation group was 145.114 (+19.961) pg/ml, stable phase group was 49.830 (+7.735) pg/ml, control group was 25.819 (+4.376) pg/ml, acute phase group was significantly higher than stable phase group, healthy control group (t = 33.34, 44.07, P 0.05), stable phase group was significantly higher than control group (t = 20.35, P 0.0.05). The serum levels of IL-6 in acute exacerbation group were 39.414+3.225 pg/ml, 32.598+3.475 pg/ml in stable phase group, 24.831+2.121 pg/ml in control group, significantly higher in acute phase group than in stable phase group, healthy control group (t = 10.81, 28.52, P 0.05), stable phase group was higher than that in control group (t = 14.31, P 0.05). 206 + 0.263 ng / ml, 2.527 + 0.469 ng / ml in stable phase group, 2.095 + 0.271 ng / ml in control group, significantly higher in acute phase group than in stable phase group (t = 8.33, 18.4, P 0.05). Respiratory function of stable phase group was significantly higher than that of control group (t = 2.69, P 0.05). 2. Respiratory function of three groups in FEV1, FEV1 / FVC was lower in acute exacerbation phase than that of stable phase group and healthy control group. The levels of serum C-reactive protein, erythrocyte sedimentation rate and D-dimer in acute exacerbation were significantly higher than those in stable and healthy control groups (P 0.05). There was no significant difference in ESR among the three groups. D-dimer in acute exacerbation was higher than that in stable and normal period. The difference was statistically significant (P 0.05). 4. The pulmonary artery diameter in the stable phase was higher than that in the healthy control group (P 0.05). The pulmonary artery pressure in the stable phase was higher than that in the stable phase (P 0.05). The pulmonary artery pressure in the stable phase was higher than that in the healthy control group (P Stable phase was higher than normal phase (P 0.05). 5. The expression of IL-21 in COPD patients with pulmonary hypertension and COPD patients without pulmonary hypertension was 273.26 (+ 23.45) pg/ml in acute exacerbation, 230.88 (+ 39.02) pg/ml in stable phase and 170.2 pg/ml in healthy control group. The results of IL-6 assay showed that the acute exacerbation stage was 37.32+4.76pg/ml, the stable stage was 34.48+4.79 pg/ml, the healthy control group was 24.73+2.13 pg/ml, the expressions of IL-21 and IL-6 in the acute exacerbation stage were significantly higher than those in the stable stage and healthy control group, and the expression of IL-6 in the stable stage was higher than that in the healthy control group (P 0.05). The mean internal diameter of pulmonary artery in the acute exacerbation stage was 26.61 (+ 2.59 mm), the stable stage was 25.51 (+ 2.34 mm) and the healthy control group was 23.72 (+ 1.89 mm). There were significant differences between the acute exacerbation stage and the stable stage and the healthy control group. Correlation analysis showed that serum IL-21 was positively correlated with IL-17, IL-6 and ROR gamma t (r = 0.795, 0.775, 0.686, P 0.05), and positively correlated with CRP (r = 0.611, P 0.05); negatively correlated with FEV1 / FVC, FEV1 (r = - 0.729, - 0.830, P 0.05); positively correlated with mean diameter of pulmonary artery and pulmonary artery pressure (r = 0.448, 0.802, P 0.05). Conclusion: 1. The expression of serum IL-21 in COPD patients was significantly increased, especially in acute exacerbation of COPD. IL-6, IL-17 and ROR-gamma T were positively correlated, suggesting that IL-21 was involved in the airway inflammation of COPD. IL-21 may play an important role in the progression of COPD through the IL-21-ROR-gamma t (TH17) -IL-17 axis. Interleukin-21 participated in the inflammatory process of COPD and played a role in promoting inflammation and bridging. 2. IL-21 was negatively correlated with airflow limitation index FEV1 / FVC, and negatively correlated with disease severity index FEV1, suggesting that IL-21 participated in the process of airflow limitation, with the increase of IL-21 expression, the disease gradually aggravated.3. COPD. The expression of IL-21 and IL-6 was significantly correlated with IL-6, mean pulmonary artery diameter and pulmonary artery pressure, suggesting that IL-21 participated in the process of pulmonary artery changes and pulmonary hypertension formation through the IL-6/IL-21 pulmonary vascular pathway.
【学位授予单位】：青岛大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R563.9
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