By Peter J. Barnes
Emphasizing the pressing have to sincerely comprehend the underlying mobile and molecular mechanisms excited by COPD, this reference presents an updated viewpoint at the inflammatory cells, mediators, and molecular pathology of COPD.
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Additional info for Chronic Obstructive Pulmonary Disease: Cellular and Molecular Mechanisms
Sample text
What is now needed is careful phenotyping and genotyping of patients to understand the cell and molecular mechanisms that determine the different patterns of pathology and progression, using a multidisciplinary approach to measure inflammation (including non-invasive markers of lung inflammation and high resolution imaging) (76). It is only through careful phenotyping of patients and longitudinal studies to follow disease progression that we will begin to understand the role of specific genes, proteins, cells, and mediators.
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Bronchial biopsies show similar changes with an infiltration of macrophages and CD8þ cells and an increased number of neutrophils in patients with severe COPD (15). Bronchoalveolar lavage (BAL) 4 Barnes fluid and induced sputum demonstrate a marked increase in macrophages and neutrophils (16,17). In contrast to asthma, eosinophils are not prominent except during exacerbations or when patients have concomitant asthma (13,18). Fixed narrowing of small airways, emphysema, and luminal obstruction with mucus secretions may all contribute to airflow limitation in COPD, but there is debate about which mechanism is most important.
