慢性阻塞性肺疾病气道上皮细胞间粘附分子1及人类白细胞抗原DR表达

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慢性阻塞性肺疾病气道炎症研究进展

气道炎症尤其小气道炎症是慢性阻塞性肺疾病的主要病变及发病的主要原因,本文就共气炎炎症的细胞学改变及细胞因子与气道炎症的关系作一简要综述,以期提高对本病的认识。     

气道炎症与慢性阻塞性肺疾病

慢性阻塞性肺疾病（ＣＯＰＤ）与哮喘均为呼吸系统的常见病和多发病,然而,明确区分或界定ＣＯＰＤ与哮喘则甚为困难。许多ＣＯＰＤ患者其表现虽与哮喘迥然不同,但是某些哮喘患者当其病程发展至晚期时亦常表现为典型的ＣＯＰＤ征象。一般认为,哮喘和ＣＯＰＤ具有各自不...     

肺泡巨噬细胞在慢性阻塞性肺疾病气道炎症中的作用

目的探讨肺泡巨噬细胞(AM)在慢性阻塞性肺疾病(COPD)气道炎症中的作用.方法收集支气管肺泡灌洗液(BALF)和支气管黏膜,用ELISA法测定BALF和AM培养上清液中巨噬细胞炎症蛋白(MIP)-lα、明胶酶B(MMP-9)及白细胞介素(IL)-8的浓度,用放射免疫法测内皮素(ET)浓度,用免疫组化法测BALF中淋巴细胞功能相关抗原1阳性(LFA-1+)AM数、黏膜内CD+/68细胞数和气道黏膜厚度.结果COPD组AM培养上清液中MIP-1α、MMP-9、ET、IL-8的浓度分别为(1446.9±126.7)μg/L、(16.98±5.15)μg/L、(43.98±5.54)ng/L、(168.10±21.22)μg/L,正常对照组为(1123.5.5±90.6)μg/L、(5.24±0.93)μg/L、(25.99±6.05)ng/L、(124.68±9.96)μg/L;COPD组支气管黏膜内CD+/68细胞数为(1.71±0.48)细胞/Hp,正常对照组为(0.59±0.18)细胞;COPD组支气管黏膜厚度为(1.96±0.96)×100-μm,正常对照组为(0.83±0.43)×10-1μg;两组比较差异均有显著性.BALF中AM数、AM培养上清液中MMP-9及ET的浓度、黏膜内CD+/68细胞数均与1秒钟用力呼气容积(FEV1)占预计值的百分比呈负相关(r=-0.511,P《0.01;r=-0.678,P《0.01;r=-0.871,P《0.01;r=-0.588,P《0.01);BALF中MIP-1α浓度、IFA-1+AM数与AM数呈正相(r=0.572,P《0.01;r=0.625,P《0.01).结论AM在COPD气道炎症和气道重建的发展过程中可能具有重要作用.     

深入研究慢性阻塞性肺疾病的气道病变

深入研究慢性阻塞性肺疾病的气道病变赵鸣武慢性阻塞性肺病（ＣＯＰＤ）是常见的、重要呼吸疾病之一，受到广泛关注，但对其防治仍有许多困难，因而也是当前呼吸内科的难题之一。近几年来，继支气管哮喘之后，ＣＯＰＤ再次引起国际呼吸病学界的重视，美国、欧洲以及新西兰...     

慢性阻塞性肺疾病气道炎症的研究近况

慢性阻塞性肺疾病气道炎症的研究近况方秋红赵鸣武慢性阻塞性肺疾病（ＣＯＰＤ）是一常见病，由于其发病率高、危害面大受到广泛重视。气道炎症，特别是小气道炎症是其主要病变特征。然而，关于气道炎症的特点、气道炎症引起慢性气道阻塞的机制并未十分明确。现将有关文献...     

实验性吸烟小鼠气道上皮细胞凋亡与慢性阻塞性疾病发生 …

细胞凋亡是细胞接受某种信号或受到某些因素刺激后主动参与的一种细胞死亡过程 ,它与疾病发生密切相关。我们采用脱氧核苷酸转移酶介导的缺口末端标记 (ＴＵＮＥＬ)技术 ,并结合透射电镜的形态学观察 ,探讨吸烟致小鼠气道上皮细胞凋亡在慢性阻塞性肺疾病 (ＣＯＰＤ)发生过程中的作用。材料与方法　 (1)动物香烟烟雾吸入实验 :健康昆明小白鼠 80只 ,体重 18～ 2 0ｇ ,每组 8只 ,共分 10组。设未吸烟对照组 3组 ,香烟烟雾吸入实验组 6组 ,余下一组动物在首次吸烟前处死作为正常对照组。实验用烟为市售红双喜牌过滤嘴香烟 (武汉卷烟厂制 ) ,尼…     

哮喘与慢性阻塞性肺疾病气道反应性研究

气道反应性增高是支气管哮喘的重要特征之一 ,是气道炎症的间接反应[1] 。气道反应性增高存在于哮喘、慢性阻塞性肺疾病 (ＣＯＰＤ)和急性呼吸道感染等疾病[2 ] 。辨别不同疾病的气道反应性及其程度对临床医生十分重要。我们对 39名健康体检者和 119例患者应用强迫振荡法连续描计呼吸阻力 ,直接记载累积激动剂量法[3 ] ,研究哮喘与ＣＯＰＤ气道反应性特征及其诊断符合率。对象与方法　将 119例患者分为两组。哮喘组 80例 :男 35例 ,女 45例 ,年龄 (4 0± 1)岁。为非急性发作期哮喘患者。ＣＯＰＤ组 39例 :男 2 1例 ,女 18例 ,年龄 (4 6± 2 …     

慢性阻塞性肺疾病大鼠模型气道重塑及生长因子的研究

目的 观察慢性阻塞性肺疾病（COPD）大鼠模型气道重塑的特点及在肺功能损害中的作用,探讨转化生长因子β1（TGF－β1）、表皮生长因子（EGF）及碱性成纤维细胞生长因子（b-FGF)与气道重塑的关系及不同药物干预的影响。方法 两次气管内注入脂多糖（LPS）及每日熏香烟的复合刺激法建立大鼠COPD模型（模型组）12只,TGF－β1单抗组6只于制作模型后第6、19d经尾静脉注射TGF－β1单抗各0．5mg。其它各药物干预组于制作模型第8d起分别雾化吸入布地奈德（布地奈德组,12只）、溴化异丙托品（溴化异丙托品组,12只）和肝素（肝素组,6只）溶液。4周后检测小支气管平滑肌及胶原厚度,用免疫组化法及原位杂交法观察各生长因子在支气管肺内的表达,用放免法检测血清和BALF中细胞外基质（ECM）成分Ⅲ型前胶原（PCⅢ）、层粘连蛋白（Ln)及透明质酸（HA）。结果 模型组小支气管平滑肌及胶原纤维较对照组增厚,其厚度均与通气功能指标0．3秒用力呼气容积（FEV0．3）呈显著负相关;模型组与TGF－β1单抗组比较,小支气管及小动脉胶原增生明显,与肝素组比较,小支气管平滑肌厚度增加。大鼠模型组血清、BALF中PCⅢ,Ln及HA均较对照组有不同程度增高;TGF－β1、EGF及b-FGF在支气管粘膜上皮等组织表达显著增强。各药物干预组PⅢ,Ln及HA在不同程度上低于模型组。结论 模型组小支气管平滑肌及胶原纤维显著增厚,构成气道重塑的主要病理基础;ECM过度沉积是COPD的显著特点,TGF－β1、EGF及b-FGF在气道重塑及肺小动脉重建中可能起重要作用,针对TGF－β1等生长因子进行干预、长期雾吸肝素,有可能为COPD气道重塑的防治提供线索。     

细胞间黏附分子-1与慢性阻塞性肺疾病的研究进展

细胞间黏附分子-1(intercellular adhesion molecule-I,ICAM-1)是黏附分子中免疫球蛋白家族中的一员,通过介导细胞-细胞、细胞-胞外基质间的黏附和相互作用,参与了机体内众多炎症反应和免疫反应过程.慢性阻塞性肺疾病(chronic 0bstructive pulmonary disea...     

慢性阻塞性肺疾病患者支气管黏膜活检标本中HO-1和iNOS的表达

目的 探讨慢性阻塞性肺疾病(COPD)患者支气管黏膜血红素氧化酶-1(HO-1)和诱生型一氧化氮合酶(iNOS)的表达及其与肺功能的关系.方法 28例因肺癌行支气管镜检查的患者,根据是否吸烟及肺功能检查分为三组:(1)吸烟伴COPD组9例;(2)吸烟肺功能正常组9例;(3)不吸烟肺功能正常组10例,经电子支气管镜钳取支气管黏膜,用免疫组化法检测支气管黏膜中HO-1和iNOS的表达,并与肺功能结果进行相关性分析.结果 吸烟伴COPD组支气管黏膜中HO-1和iNOS的表达(0.156±0.036,0.188±0.030)较不吸烟肺功能正常组(0.094±0.043,0.159±0.034)明显增强,差异有统计学意义(P＜0.01);吸烟伴COPD组和吸烟肺功能正常组(0.147±0.049 vs 0.176±0.053)之间没有统计学差异(P＞0.05).气管黏膜中HO-1和iNOS的表达无相关性(r=0.046,P＞0.05).气管黏膜中HO-1的表达与FEV1呈负相关(r=-0.558,P ＜0.05).结论 COPD患者气管黏膜中HO-1和iNOS的表达增强,并且与FEV1呈负相关.     

Increased LHX9 expression in alveolar epithelial type 2 cells of patients with chronic obstructive pulmonary disease

BackgroundAlveolar epithelial type 2 (AT2) cells serve as stem cells in alveolar epithelium and are assumed to lose their stem cell function in the lungs of chronic obstructive pulmonary disease (COPD). Although we previously reported that LHX9 mRNA expression was up-regulated in AT2 cells of COPD lung tissues, it is yet to be elucidated how LHX9 is associated with the vulnerability of AT2 cells in COPD.MethodsAT2 cells were isolated from lung tissues of 10 non-COPD subjects and 11 COPD patients. LHX9 mRNA expression was determined by quantitative RT-PCR. To identify up-stream molecules, an alveolar epithelial cell line A549 was exposed to pro-inflammatory cytokines in vitro. siRNA-mediated Lhx9 knockdown was performed to determine how Lhx9 affected the cellular viability and the cell-division cycle.ResultsLHX9 mRNA expression was increased in AT2 cells from COPD lung tissues, compared to those from non-COPD tissues. The airflow obstruction was independently correlated with the increase in LHX9 expression. Among several pro-inflammatory cytokines, interferon-γ was a strong inducer of LHX9 expression in A549 cells. Lhx9 was involved in the increased susceptibility to serum starvation-induced death of A549 cells.ConclusionsOur data suggest that IFN-γ predominantly increases the LHX9 expression which enhances the susceptibility to cell death. Considering the independent association of the increased LHX9 expression in AT2 cells with airflow obstruction, the IFN-γ-Lhx9 axis might contribute to the vulnerability of AT2 cells in the lungs of COPD patients.     

前列环素在慢性阻塞性肺疾病患者肺组织中的表达

目的 研究前列环素在慢性阻塞性肺疾病患者肺组织中的表达变化.方法 分别采集湘雅二医院2008年6-10月因肺癌、肺大疱入院行肺叶切除术的患者22例的肺组织标本,分为COPD组(12例)和对照组(10例).采用缺口末端标记法定量测定肺血管内皮细胞凋亡,免疫组织化学法检测前列环素合酶(PGI_2-S)蛋白表达,酶联免疫吸附试验测定6-酮前列腺素F_(1α)含量变化.两组间比较采用t检验.结果 COPD组肺中型血管和微小型血管内皮细胞凋亡指数[(12.9±2.0)%和(11.4±1.4)%]明显高于对照组[(6.1±1.2)%和(5.9±0.4)%],PGI_2-S蛋白表达率[(55.2±9.8)%和(42.3±5.1)%]明显低于对照组[(95.4±2.1)%和(82.3±7.4)%],气道上皮细胞中PGI_2-S蛋白表达率[(31.8±5.2)%]明显低于对照组[(95.5±2.2)%],6-酮前列腺素F_(1α)含量[(2.6±0.4)μg/L]明显低于对照组[(16.2±2.8)μg/L],差异均有统计学意义(t值为9.6～173.6,均P<0.01).结论 COPD患者肺血管内皮细胞存在异常凋亡现象,PGI_2-S蛋白表达下降,肺组织中前列环素生成明显减少,这些变化可能是COPD患者肺血管内皮细胞功能异常的组织学标志,并参与COPD的发生与发展.     

Respiratory rehabilitation in patients with bronchial asthma and chronic obstructive pulmonary disease (COPD) in Kinshasa]

A number of studies in western countries have shown that respiratory and physical rehabilitation of patients with chronic obstructive pulmonary disease (COPD) only has a minimal effect on respiratory function but can significantly improve physical capacity. The aim of our study was to apply these methods to patients in Kinshasa, Democratic Republic of Congo. We treated 38 patients (20 women) who had bronchial asthma (n=14) or COPD (n=24). These ambulatory patients were treated in two different hospitals in Kinshasa, the university hospital and the general hospital, three times per week for twelve weeks. The patients were treated with kinestherapy and inhaled bronchodilator drugs (salbutamol, and/or ipratropium bromide with a boreal nebulizer) as well as bronchial hygiene and performed breathing exercises on a Bodyguard Ergometer 990 with walking, running and climbing steps until exhaustion. After the rehabilitation program FEV1 increased from 1.37 +/- 0.62 (50% expected) to 1.54 +/- 0.69 (56% expected) (p<0.01). The same trend was observed for walking distance (from 644 +/- 459 m to 1213 +/- 569 m, p<0.001) and for maximal power developed on the cycloergometer (from 45 +/- 20 w to 73 +/- 37 w, p<0.001). In contrast, the maximal work load performed during climbing steps (from 106 +/- 44 w to 115 +/- 23 w) did not improve significantly. COPD patients improved their FEV1 significantly compared with asthma patients. Our study show that pulmonary rehabilitaion increase the level of spontaneous physical activity. The pulmonary rehabilitation program changes the quality of life of COPD patients who are able to move about better for longer periods of time, have a longer walking distance, and improved physical activity level.