文摘
的又一个主要因素的发展,慢性阻塞性肺疾病(COPD)是香烟的炎症反应。然而,当那些慢性阻塞性肺病停止吸烟,一个连续的循环炎症可以导致肺功能持续下降。理解炎症细胞的作用在慢性阻塞性肺病是困难的,因为它是一个混合的疾病,支气管炎,小气道疾病和肺气肿——炎症表现出不同的模式和不同的病理。中性粒细胞和巨噬细胞参与这个过程;他们释放蛋白水解酶和产生氧化剂,导致组织损伤,以及细胞因子和趋化因子,它可以加强炎症和引发免疫反应。分析痰及支气管肺泡灌洗液显示增加中性粒细胞和巨噬细胞在慢性阻塞性肺病的呼吸道分泌物的主题;中性粒细胞中的主要细胞进行航空公司,而巨噬细胞是主要从小型航空公司和薄壁组织细胞分泌物。气道组织中性粒细胞增加在大型和小型航空公司在感染和急性加重,而实质中性粒细胞数量肺泡壁破坏成反比,这表明他们不参与肺气肿的进展。巨噬细胞增加整个呼吸道气道腔和上皮细胞在慢性阻塞性肺病和疾病严重程度正相关,气道阻塞和肺气肿的肺泡壁的破坏程度。未激活的t淋巴球不停留在肺部组织。 Activated (eg due to antigenic stimulus) memory T cells home in to the lung and act as effector cells. CD-8+ T cell differentiation into memory cells is facilitated by CD4+ T cells. Binding of CD-8+ T cells to collagen stimulates proliferation and mediator production which may contribute to the inflammatory response. CD8+ cytotoxic/suppressor T cells release cytotoxic perforins and granzyme B which cause cell death and apoptosis, a feature of emphysema. Lung secretions contain only a small percentage of T cells; most Tlymphocytes reside in the subepithelial and smooth muscle region of the tissue. During COPD, there is either an increase in the CD8+/CD4+ ratio of T cells, or an increase in the in total numbers of both CD8+ and CD4+ T cells, in the tissue. Smoking status, smoking history, degree of airway obstruction and emphysema are all related to increased CD8+ cells and/or CD8+/CD4+ ratio. During severe emphysema requiring lung volume reduction surgery, there is a considerable increase in macrophages, neutrophils, eosinophils, CD4+ and CD8+ T cells which relates to the severity of the disease. Interestingly, the marked increase in luminal CD8+ cells results in an increased ratio of CD8+/CD4+ T cells that is not seen in the parenchymal tissue. The florid inflammation observed in severe emphysema is suggested to be related to latent viral infection.
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