Chronic obstructive pulmonary disease (COPD) is a complex inflammatory disease that involves multiple interacting cells and mediators and various tissue destruction and repair mechanisms leading to structural changes that result in progressive airflow limitation with little reversibility. The links between the cellular and molecular mechanisms, the pathology, the physiological abnormalities, and symptoms are still not well understood. This is complicated by the fact that there is heterogeneity of the disease, with some patients showing a predominant emphysema pattern, whereas in others small airway disease predominates, although many patients have a mixed pattern, as cigarette smoking is a common causal mechanism. Although the commonest cause of COPD is chronic cigarette smoking, some patients, particularly in developing countries, develop the disease from inhalation of wood smoke from biomass fuels or other inhaled irritants. However, only about 25% of smokers develop COPD of at least moderate severity. The disease is thought to be relentlessly progressive and, to date; only smoking cessation has been demonstrated to reduce the rate of decline in lung function, although as the disease becomes more severe there is less effect of smoking cessation and lung inflammation persists. However, it is not yet clear that all patients with mild and moderate COPD show progression. The role, played by structural cells in responding to inflammatory cell-mediated injury and the degree to which it is deficient in COPD remains to be fully defined. More research into these mechanisms is needed in order to identify novel targets that may lead to the discovery of more effective therapies that are able to prevent disease progression and reduce the high mortality of this common disease.
|Original language||English (US)|
|Title of host publication||Asthma and COPD|
|Number of pages||18|
|Publication status||Published - Dec 1 2009|
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