O'Shaughnessy T C, Ansari T W, Barnes N C, Jeffery P K
Lung Pathology Unit, Imperial College, London, United Kingdom.
Am J Respir Crit Care Med. 1997 Mar;155(3):852-7. doi: 10.1164/ajrccm.155.3.9117016.
In order to determine whether the airway inflammatory cells of chronic obstructive pulmonary disease (COPD) are different from those seen in asthma, we have studied a subepithelial zone, 100 microns deep to the epithelial reticular basement membrane in bronchial biopsies taken from five normal nonsmoking subjects without chronic bronchitis or asthma (FEV1 percentage of predicted [mean +/- SD] 105.7 +/- 25.3), 11 subjects with chronic bronchitis alone (FEV1 percentage of predicted 98.5 +/- 12.9), and 13 subjects with chronic bronchitis in whom there was also evidence of airflow limitation (i.e., COPD; FEV1 percentage of predicted 59.7 +/- 10.0). Using immunohistochemical markers, we counted distinct types of inflammatory cell and expressed them as [median and range] per mm basement membrane. When there was airflow limitation we found significantly increased numbers of CD3+ T lymphocytes (COPD 22.3 [2.6 to 68.2] versus normal 3.7 [1.5 to 16.3]; p < 0.05), an increased number of CD8+ cells (COPD 19.3 [1.8 to 45.5] versus normal 2.3 [0.9 to 4.2]; p < 0.01), and increased expression of HLA-DR (COPD versus normal; p = 0.01). There was also an increased number of CD68+ cells (i.e., macrophages) (COPD 7.4 [0.4 to 16.9] versus normal 0.7 [0 to 2.6]; p < 0.01; COPD versus chronic bronchitis alone 2.7 [0 to 12.8]; p < 0.05). There were no significant differences between the groups in the numbers of subepithelial neutrophils, mast cells, eosinophils or B lymphocytes. There were weak but significant negative associations between the CD8+ T-cell subset (r = -0.42), neutrophils (r = -0.46), and eosinophils (r = -0.53) and FEV1 percentage of predicted in all the chronic bronchitic smokers (p < 0.05). The data confirm the involvement of subepithelial T lymphocytes and macrophages in smoking-induced airflow limitation and provide novel data which support the view that COPD is distinct from asthma with respect to the predominance of the CD8+ T-cell subset in this smoking-related condition.
为了确定慢性阻塞性肺疾病（COPD）的气道炎症细胞是否与哮喘患者不同，我们研究了五个无慢性支气管炎或哮喘的正常非吸烟受试者（预测FEV1百分比[均值±标准差]为105.7±25.3）、11名仅患有慢性支气管炎的受试者（预测FEV1百分比为98.5±12.9）以及13名同时有气流受限证据的慢性支气管炎患者（即COPD；预测FEV1百分比为59.7±10.0）支气管活检标本中上皮下区域，该区域位于上皮网状基底膜下方100微米深处。使用免疫组化标记物，我们对不同类型的炎症细胞进行计数，并将其表示为每毫米基底膜的[中位数和范围]。当存在气流受限时，我们发现CD3 + T淋巴细胞数量显著增加（COPD为22.3[2.6至68.2]，而正常人为3.7[1.5至16.3]；p<0.05），CD8 +细胞数量增加（COPD为19.3[1.8至45.5]，而正常人为2.3[0.9至4.2]；p<0.01），HLA - DR表达增加（COPD与正常相比；p = 0.01）。CD68 +细胞（即巨噬细胞）数量也增加（COPD为7.4[0.4至16.9]，而正常人为0.7[0至2.6]；p<0.01；COPD与仅患有慢性支气管炎相比为2.7[0至12.8]；p<0.05）。各组上皮下中性粒细胞、肥大细胞、嗜酸性粒细胞或B淋巴细胞数量无显著差异。在所有慢性支气管炎吸烟者中，CD8 + T细胞亚群（r = -0.42）、中性粒细胞（r = -0.46）和嗜酸性粒细胞（r = -0.53）与预测FEV1百分比之间存在微弱但显著的负相关（p<0.05）。这些数据证实上皮下T淋巴细胞和巨噬细胞参与了吸烟引起的气流受限，并提供了新的数据支持以下观点：在这种与吸烟相关的疾病中，COPD在CD8 + T细胞亚群的优势方面与哮喘不同。
