Many cells have been reported to be involved in the pathogenesis of COPD. However, their presence or activation in the affected tissues, or in fluids such as sputum or bronchoalveolar lavage (BAL), does not necessarily confirm their role in the process of disease development. The number of macrophages is increased in COPD . Cigarette smoke also activates macrophages to release mediators, including IL-8, leukotriene B4 (LTB4) and TNF-a . Thus, macrophages may orchestrate the inflammation process in COPD.
Neutrophils are the cells that have been studied most in COPD, but their role is not yet clear [22-24]. Neutrophils cause elastolysis by secreting neutrophil elastase, cathepsin G and proteinase 3 . In addition, neutrophil proteases are mucus stimulants. Recruitment of neutrophils is the result of potent chemotaxis by IL-8, LTB4 and increased adherence (Mac-1, E-selectin) . Neutrophilic survival in the respiratory tract is increased in COPD by the increase of cytokines, such as granulocyte-macrophage colony-stimulating factor (GM-CSF). Although neutrophils are increased and/or activated in other diseases, such as cystic fibrosis, their elastolytic effect is not as prominent as in COPD. Other factors may therefore be involved in promoting the elastolytic activity of neutrophils in COPD .
T lymphocytes are increased in lung parenchyma, and in both peripheral and central airways in COPD [28,29]. In contrast to asthma, in which the CD4 cell is prominent in the airway, CD8+ cells are increased in the airway mucosa in COPD patients and may cause cytolysis and apoptosis of alveolar epithelial cells [29,30]. Although there is an association between T lymphocytes and the amount of alveolar destruction and airflow limitation [28,31] the role of T cells in the pathogenesis of COPD is not yet certain.
Although eosinophils play an important part in the mechanisms of airway inflammation in asthma, their role in COPD is obscure. There are conflicting reports concerning their numbers in stable disease, but most reports have shown an increase during exacerbations [32-34]. Their interaction with neutrophils and their degranulation are also under investigation.
It has recently been shown that airway epithelial cells are of importance in secreting inflammatory mediators. Cigarette smoke activates epithelial cells to produce TNF-a and IL-8and may therefore initiate the abnormal inflammatory response . Many inflammatory mediators may be involved in the pathogenesis of COPD; the most important ones that have been described are the lipid mediator LTB4, the chemokine IL-8 and the cytokine TNF-a [21,33,35-37]. Other mediators that have been reported to have inflammatory effects in COPD include IL-5, GM-CSF, transforming growth factor-b (TGF-b), epidermal growth factor (EGF), endothelin-1 (ET-1) [33,38-40]. The inflammatory response in COPD may be up-regulated by a combination of the above mediators.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.