Inflammation of the airways and lung parenchyma in COPD
Inflammation of the airways and lung parenchyma in COPD
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DOI：
10.1378/chest.121.5_suppl.160s
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发表时间：
2002-05-01
期刊：
影响因子：
9.6
通讯作者：
Cosio, MG
中科院分区：
文献类型：
--
作者：
Cosio, MG;Majo, J;Cosio, MG
吸烟引起的气道和肺实质炎症反应，主要由中性粒细胞和肺泡巨噬细胞组成，长期以来被认为是吸烟者COPD的主要原因。最近的报道强调了T淋巴细胞在导致慢性阻塞性肺病的炎症过程中的潜在重要因素的作用。已经发现，在气道和肺实质中，T细胞的存在，主要是CD8+ T细胞，可以区分患有和非COPD的吸烟者。除T细胞外，其他炎症细胞类型，如中性粒细胞和巨噬细胞，在导致肺组织破坏的初始炎症过程中可能是必不可少的，可能产生最终被T细胞识别为抗原的肽。这将为t细胞炎症提供一个解释。一旦被激活，T细胞就会出现在肺中，它们的效应功能包括吸引和增强其他炎症细胞（如中性粒细胞和巨噬细胞）的炎症功能。似乎只有当肺中存在所有炎症细胞类型（即CD4+、CD8+、中性粒细胞和巨噬细胞）时，才会发生COPD特征的气道重塑和实质破坏。如果T细胞对肺损伤和COPD的进展负责，它将类似于对源自肺部的抗原刺激的反应。如果是这样的话，慢性阻塞性肺病可以被认为是一种由吸烟引发的自身免疫性疾病。
A smoking-induced inflammatory reaction in the airways and lung parenchyma, comprised mainly of neutrophils and alveolar macrophages, has long been accepted to be the major cause of COPD in smokers. Recent reports have underlined the role of the T lymphocyte as a potentially important factor in the inflammatory process leading to COPD. it has been found that, in the airways and the lung parenchyma, the presence of T cells, predominantly CD8+ T cells, can distinguish between smokers with and without COPD. In addition to T cells, other inflammatory cell types such as neutrophils and macrophages are probably essential in the initial inflammatory process leading to the breakdown of lung tissue, perhaps producing peptides eventually recognized by T cells as antigenic. This would provide an explanation for the T-cell inflammation. Once activated, T cells are present in the lung, and their effector functions would include the attraction and enhancement of the inflammatory function in other inflammatory cells like neutrophils and macrophages. It seems likely that, only when all inflammatory cell types (ie, CD4+, CD8+, neutrophils, and macrophages) are present in the lung, the airways remodeling and parenchymal destruction characteristic of COPD will ensue. If T cells are responsible for the lung injury and progression of COPD, it would resemble a response to an antigenic stimulus originating in the lung. If that were the case, COPD could be considered to be an autoimmune disease triggered by smoking.