Corrigan C J, Kay A B
Department of Allergy and Clinical Immunology, National Heart & Lung Institute, London, United Kingdom.
Am Rev Respir Dis. 1991 May;143(5 Pt 1):1165-8; discussion 1175-6. doi: 10.1164/ajrccm/143.5_Pt_1.1165.
Studies of the inflammatory processes in asthma and in COPD have been hindered by the imprecise definitions of these diseases, the uncertainty as to the location of the relevant inflammatory sites for these diseases within the lungs, and the difficulties in relating observed histopathologic changes to the effects of particular proinflammatory leukocytes or their products. Circumstantial evidence exists implicating neutrophils, eosinophils, mast cells, and monocytes in asthma pathogenesis based on increased numbers and activation of these cells in blood, BAL fluid, or biopsy material, and the propensity of these cells to release products causing tissue damage. There is increasing evidence that the accumulation and activation of these cells is orchestrated by lymphokines elaborated by sensitized T lymphocytes. In COPD, attention has been focused on the secretion of proteases by infiltrating neutrophils and macrophages, although there is no incontrovertible evidence that these are relevant to the disease pathogenesis in the majority of patients with normal serum concentrations of protease inhibitors. In the future, studies of the functions of inflammatory cells actually at the sites of inflammation using the techniques of immunocytochemistry and molecular biology may provide further information as to the role of these cells in the inflammatory processes associated with asthma and COPD.
哮喘和慢性阻塞性肺疾病（COPD）炎症过程的研究受到多种因素的阻碍，包括这些疾病定义不精确、肺部相关炎症部位位置不确定，以及难以将观察到的组织病理学变化与特定促炎白细胞或其产物的作用联系起来。有间接证据表明，基于血液、支气管肺泡灌洗（BAL）液或活检材料中这些细胞数量的增加和激活，以及这些细胞释放导致组织损伤产物的倾向，中性粒细胞、嗜酸性粒细胞、肥大细胞和单核细胞参与了哮喘的发病机制。越来越多的证据表明，这些细胞的聚集和激活是由致敏T淋巴细胞分泌的淋巴因子所调控的。在COPD中，注意力主要集中在浸润的中性粒细胞和巨噬细胞分泌蛋白酶上，尽管在大多数蛋白酶抑制剂血清浓度正常的患者中，没有确凿证据表明这些蛋白酶与疾病发病机制相关。未来，使用免疫细胞化学和分子生物学技术对炎症实际部位的炎症细胞功能进行研究，可能会提供更多关于这些细胞在哮喘和COPD相关炎症过程中作用的信息。
