Chronic Obstructive Pulmonary Disease: Cellular and by Peter J. Barnes

By Peter J. Barnes

Emphasizing the pressing have to essentially comprehend the underlying mobile and molecular mechanisms focused on COPD, this reference presents an up to date point of view at the inflammatory cells, mediators, and molecular pathology of COPD.

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Additional resources for Chronic Obstructive Pulmonary Disease: Cellular and Molecular Mechanisms

Example text

The destruction of alveolar attachments allows the airway wall to deform, thus narrowing the airway lumen and therefore contributing to airflow obstruction. COPD is a progressive disease that in a minority of subjects may worsen toward a very severe stage. Investigating these patients may be of interest because a better characterization of their lung pathology may help to clarify why, among patients with a similar smoking history, only a minority develop a severe disease. Furthermore, even if patients with severe COPD 24 Turato et al.

Rather than this representing a graded spectrum of disease, it is more likely that these patients have both of these common diseases at the same time. A. Differences from Asthma Histopathological studies of COPD show a predominant involvement of peripheral airways (bronchioles) and lung parenchyma, whereas asthma involves inflammation in all airways but usually without involvement of the lung parenchyma (13). There is obstruction of bronchioles, with fibrosis and infiltration with macrophages and T-lymphocytes.

Indeed, the extent of lung inflammation appears to progressively increase from smokers with normal lung function to smokers with severe COPD (10,14,15). Although the hypothesis is attractive, convincing evidence that the development of structural changes is dependent on the prior development of chronic inflammation is still lacking (16). It seems equally plausible that structural changes could arise regardless of chronic inflammation. Although the mechanisms of individual susceptibility to the development of COPD are not completely understood, a possible explanation for the amplification of the inflammatory response in susceptible smokers could be an altered production of inflammatory mediators.

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