COPD病人T淋巴细胞和细胞因子的检测及意义
摘要
慢性阻塞性肺疾病是一种气道炎症性疾病,具有气流受限特征,且气流受限不完全可逆,呈持续进行性发展。它与肺部对香烟烟雾等有害气体或有害颗粒的异常炎症反应有关。早期患者一般无明显的病理生理改变,随着疾病的进一部演变,逐渐出现气道狭窄、气道阻塞、气流受限。肺泡过度通气,肺泡壁大量断裂,肺泡毛细血管破坏而大量减少,使肺泡壁无血液灌流,不能正常进行气体交换,肺功能进行性减退,引起缺氧和二氧化碳储留,出现低氧血症和高碳酸血症,严重影响患者生活质量,许多病人最终因呼吸衰竭或慢性肺源性心脏病而死亡。COPD由于其患病人数多,死亡率高,造成巨大的社会负担和经济负担,已成为一个重要的公共卫生问题。
COPD患者戒烟后肺内炎症持续存在,可能是包括炎症在内的复合因素最终决定了疾病进展。COPD的炎症过程中有中性粒细胞、巨噬细胞、T淋巴细胞及多种细胞因子、炎症介质参与,有学者提出COPD是自身免疫性疾病的假设。本文第一部分采用免疫荧光双标记法和流式细胞仪检测COPD患者外周血中的T淋巴细胞及其亚群,结果显示:与健康对照组相比较,(1)急性期COPD组的CD3+T细胞及CD4 +T细胞亚群下降,CD8~+ T亚群细胞升高,导致CD4~+/ CD8~+比值下降并倒置;(2)CD4~+CD45RA~+亚群、CD4~+CD45RA~+/CD4~+CD45RO~+比值下降,CD4~+CD45RO~+亚群上升;(3)CD8~+CD45RA~+亚群、CD8~+CD45RO~+亚群与CD8~+CD45RA~+/CD8~+CD45RO~+比值均有所上升;(4)自身免疫性疾病有关的CD4~+CD28~+亚群下降。上述结果提示COPD患者体内存在细胞免疫功能的紊乱。
本文第二部分采用ELISA法检测COPD患者外周血中与炎症有关的因子,结果显示(:1)急性期COPD组与健康对照组和缓解期组相比较,促炎细胞因子IL-1β、IL-6、IL-8、TNF-α以及hs-CRP显著升高,差异具有统计学意义(P<0.05);(2)急性期COPD组的抗炎细胞因子IL-10显著低于健康对照组(P<0.05),亦低于缓解期组,提示上述炎症相关因子参与了COPD的炎症过程。
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease. It characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases. No obvious patho-physiological changes in early stage for patients existed. As the disease evolved, the slowly progressive development of airflow limitation and obstruction occurred. The enlargement of airspaces and destruction of alveolar walls reduced severely alveolar capillary, resulting in no blood flows and air changes for alveolar walls. The regression of lung function induced hypoxia, carbon dioxide retention. The hypoxemia and hypercapnia followed, affecting living quality of COPD patients, many of whom died of respiratory failure and chronic cor pulmonale. As a commonest disease, with high death rate, enormous burden of disease and escalating healthcare costs, COPD is becoming an important public health problem.
It was shown after the further research that their lung inflammation would still exist even if the COPD patients stopped smoking. So, it is possibly the composite factor including inflammation that finally determines the progress of COPD. In addition to several cytokines, neutrophils, macrophages and T lymphocytes were involved in the inflammatory progress of COPD. Some doctors assume that COPD is an autoimmune disease.
In the first part of this report, T lymphocytes and their subsets in peripheral blood of COPD patients were examined by using double immunofluorescence labeling and flow cytometry. The results showed that: compared with normal control subjects, (1) CD3+T lymphocytes and CD4~+T subsets in acute exacerbating COPD patients were decrease,CD8~+ T subsets was increase,with the ratio of CD4~+/ CD8~+ being decreased and inverted;(2) CD4~+CD45RA~+ subsets and CD4~+CD45RA~+/CD4~+CD45RO~+ were decrease, CD4~+CD45RO~+ subsets was increase; (3) CD8~+CD45RA~+ subsets, CD8~+CD45RO~+ subsets and CD8~+CD45RA~+/CD8~+CD45RO~+ were increase;(4) the autoimmune disease related CD4~+CD28~+ subsets was decrease. These results suggested that the dysfunction of cellular immunity existed in COPD patients.
In the second part of this report, the inflammation related factors in peripheral blood of COPD patients were determined by using ELISA. The results showed that: (1) the concentration of IL-1β, IL-6, IL-8, IL-10, TNF-αand hs-CRP in acute exacerbating COPD patients was greatly increased compared with those paracmasis COPD patients and normal control subjects. The difference is of significance in statistics (P<0.05); (2) the concentration of anti- inflammatory cytokines IL-10 in acute exacerbating COPD patients was lower than not only the normal control subjects (P<0.05), but also the paracmasis COPD patients, suggesting that these inflammation associated factors were involved in the inflammatory progress of COPD.
COPD患者戒烟后肺内炎症持续存在,可能是包括炎症在内的复合因素最终决定了疾病进展。COPD的炎症过程中有中性粒细胞、巨噬细胞、T淋巴细胞及多种细胞因子、炎症介质参与,有学者提出COPD是自身免疫性疾病的假设。本文第一部分采用免疫荧光双标记法和流式细胞仪检测COPD患者外周血中的T淋巴细胞及其亚群,结果显示:与健康对照组相比较,(1)急性期COPD组的CD3+T细胞及CD4 +T细胞亚群下降,CD8~+ T亚群细胞升高,导致CD4~+/ CD8~+比值下降并倒置;(2)CD4~+CD45RA~+亚群、CD4~+CD45RA~+/CD4~+CD45RO~+比值下降,CD4~+CD45RO~+亚群上升;(3)CD8~+CD45RA~+亚群、CD8~+CD45RO~+亚群与CD8~+CD45RA~+/CD8~+CD45RO~+比值均有所上升;(4)自身免疫性疾病有关的CD4~+CD28~+亚群下降。上述结果提示COPD患者体内存在细胞免疫功能的紊乱。
本文第二部分采用ELISA法检测COPD患者外周血中与炎症有关的因子,结果显示(:1)急性期COPD组与健康对照组和缓解期组相比较,促炎细胞因子IL-1β、IL-6、IL-8、TNF-α以及hs-CRP显著升高,差异具有统计学意义(P<0.05);(2)急性期COPD组的抗炎细胞因子IL-10显著低于健康对照组(P<0.05),亦低于缓解期组,提示上述炎症相关因子参与了COPD的炎症过程。
Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease. It characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases. No obvious patho-physiological changes in early stage for patients existed. As the disease evolved, the slowly progressive development of airflow limitation and obstruction occurred. The enlargement of airspaces and destruction of alveolar walls reduced severely alveolar capillary, resulting in no blood flows and air changes for alveolar walls. The regression of lung function induced hypoxia, carbon dioxide retention. The hypoxemia and hypercapnia followed, affecting living quality of COPD patients, many of whom died of respiratory failure and chronic cor pulmonale. As a commonest disease, with high death rate, enormous burden of disease and escalating healthcare costs, COPD is becoming an important public health problem.
It was shown after the further research that their lung inflammation would still exist even if the COPD patients stopped smoking. So, it is possibly the composite factor including inflammation that finally determines the progress of COPD. In addition to several cytokines, neutrophils, macrophages and T lymphocytes were involved in the inflammatory progress of COPD. Some doctors assume that COPD is an autoimmune disease.
In the first part of this report, T lymphocytes and their subsets in peripheral blood of COPD patients were examined by using double immunofluorescence labeling and flow cytometry. The results showed that: compared with normal control subjects, (1) CD3+T lymphocytes and CD4~+T subsets in acute exacerbating COPD patients were decrease,CD8~+ T subsets was increase,with the ratio of CD4~+/ CD8~+ being decreased and inverted;(2) CD4~+CD45RA~+ subsets and CD4~+CD45RA~+/CD4~+CD45RO~+ were decrease, CD4~+CD45RO~+ subsets was increase; (3) CD8~+CD45RA~+ subsets, CD8~+CD45RO~+ subsets and CD8~+CD45RA~+/CD8~+CD45RO~+ were increase;(4) the autoimmune disease related CD4~+CD28~+ subsets was decrease. These results suggested that the dysfunction of cellular immunity existed in COPD patients.
In the second part of this report, the inflammation related factors in peripheral blood of COPD patients were determined by using ELISA. The results showed that: (1) the concentration of IL-1β, IL-6, IL-8, IL-10, TNF-αand hs-CRP in acute exacerbating COPD patients was greatly increased compared with those paracmasis COPD patients and normal control subjects. The difference is of significance in statistics (P<0.05); (2) the concentration of anti- inflammatory cytokines IL-10 in acute exacerbating COPD patients was lower than not only the normal control subjects (P<0.05), but also the paracmasis COPD patients, suggesting that these inflammation associated factors were involved in the inflammatory progress of COPD.
引文
1. Peter J Barnes, S D Shapiro, R A Pauwels. Chronic obstructive pulmonary disease: molecular and cellular mechanisms. Eur Respir J,2003,22:672-688.
2. Lopez AD, Murray CC. The global burden of disease, 1990-2020. Nat Med, 1998, 4:1241-1243.
3. Anna M. Stefanska and Patrick T. Walsh. Chronic Obstructive Pulmonary Disease: Evidence for an Autoimmune Component. Cellular & Molecular Immunology,2009,6(2):81-86.
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6.杜晓华,李为民.炎性因子在慢性阻塞性肺疾病急性加重期的作用研究.临床肺科杂志,2008,13(11):1399-1402.
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10. Peter J Barnes. Immunology of asthma and chronic obstructive pulmonary disease. Nature Reviews Immunology,2008, 8:183-192.
11. Pilette C, Ouadrhiri Y, Godding V, Vaerman JP, Sibille Y. Lung mucosal immunity: immunoglobulin-A revisited. Eur Respir J, 2001, 18:571-588.
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1. Peter J Barnes. Immunology of asthma and chronic obstructive pulmonary disease. Nature Rev Immunology, 2008, 8:183-192.
2. Anna M. Stefanska and Patrick T. Walsh. Chronic Obstructive Pulmonary Disease: Evidence for an Autoimmune Component. Cellular & Molecular Immunology,2009, 6(2): 81-86.
3. Peter J Barnes, S D Shapiro, R A Pauwels. Chronic obstructive pulmonary disease: molecular and cellular mechanisms. Eur Respir J, 2003, 22:672-688.
4.许力军,唐颖,吴英慧等.联合吸入治疗对AECOPD患者外周T淋巴细胞、IL-2、CRP表达的调节以及肺功能的影响.中国现代医学杂志, 2009,19(7): 1035-1038.
5.万鹏,钟小宁.免疫反应与慢性阻塞性肺疾病.中国实用内科杂志, 2009,29(4):371-373.
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2. Lopez AD, Murray CC. The global burden of disease, 1990-2020. Nat Med, 1998, 4:1241-1243.
3. Anna M. Stefanska and Patrick T. Walsh. Chronic Obstructive Pulmonary Disease: Evidence for an Autoimmune Component. Cellular & Molecular Immunology,2009,6(2):81-86.
4.黄绍光.自身免疫在慢性阻塞性肺病的作用.上海交通大学学报(医学版),2008,28(9):1062-1064.
5.中华医学会呼吸病学分会.慢性阻塞性肺疾病(COPD)诊治指南.中华结核和呼吸杂志,2007,30(1):8-17.
6.杜晓华,李为民.炎性因子在慢性阻塞性肺疾病急性加重期的作用研究.临床肺科杂志,2008,13(11):1399-1402.
7.中华医学会呼吸病学分会.慢性阻塞性肺疾病学组,慢性阻塞性肺疾病诊治指南(2007年修订版).中华内科杂志,2007,46(3):254-261.
8. COPD全球倡议执行委员会.COPD全球倡议(2006)解读.继续医学教育,2007,21(2):1-8.
9.万鹏,钟小宁.免疫反应与慢性阻塞性肺疾病.中国实用内科杂志,2009,29(4):371-373.
10. Peter J Barnes. Immunology of asthma and chronic obstructive pulmonary disease. Nature Reviews Immunology,2008, 8:183-192.
11. Pilette C, Ouadrhiri Y, Godding V, Vaerman JP, Sibille Y. Lung mucosal immunity: immunoglobulin-A revisited. Eur Respir J, 2001, 18:571-588.
12. Di Stefano A, Caramori G, Capelli A, et al. Increased expression of NF-κB in bronchial bioipsies from smokers and patients with COPD. Eur Respir J, 2002, 20:556-563.
13. Caramori G, Romagnoli M, Casolari P, et al. Nuclear localization of p65 in sputum macrophages but not in sputum neutrophils during COPD exacerbations. Thorax, 2003, 58:348-351.
14.王春兰,刘晓民,李丽娜.慢性阻塞性肺疾病患者血清白介素-17、基质金属蛋白酶-9水平测定及其意义.黑龙江医药, 2008, 21(3): 49-51.
15.杨捷,冯玉麟.树突状细胞与慢性阻塞性肺病.国际内科学杂志, 2009, 36(7): 432-434.
16. Vestbo J, Prescott E, Lange P. Association of chronic mucus hypersecretion with FEV1 decline and chronic obstructive pulmonary disease morbidity. Copenhagen City Heart Study Group. Am J Reapir Crit Care Med, 1996, 153:1530-1535.
17. Vestbo J. Epidemiological studies in mucus hypersecretion. Novartis Found Symp, 2002, 248:3-12.
18. Takubo Y, Guerassimov A, Ghezzo H, et al. Alphalantitrypsin determines the pattern of emphysema and function in tobacco smoke-exposed mice: parallels with human disease. Am J Respir Care Med, 2002, 166:1596-1603.
19.龚燕,金美玲,任涛,等.肿瘤坏死因子α与慢性阻塞性肺疾病相关性研究.中国康复理论与实践,2008,14(6).
20.许力军,唐颖,吴英慧,等.联合吸入治疗对AECOPD患者外周T淋巴细胞、IL-2、CRP表达的调节以及肺功能的影响.中国现代医学杂志, 2009,19(7):1035-1038.
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