Diagnosis and Disease Staging COPD

In asthma, inhaled allergens encounter dendritic cells that line the airway, and these cells migrate to draining lymph nodes where they present processed allergen (antigen) to T- and Bcells. The B-cells are induced through a complex series of costimulatory signals to produce IgE, which binds to high-affinity receptors on the surface of mast cells in tissue. When the allergen subsequently interacts with the receptor-bound IgE molecules, activation and degranulation of the mast cells occur, resulting inrelease of histamine and leukotrienes, and causing smooth muscle constriction that results in the early-phase airway obstruction seen in asthma.5 Prolonged, late-stage reactions develop as a result of the release of cytokines and chemokines (IL-4, IL-5, IL-13) generated by the resident inflammatory cells in the lung
(Table 1).5

These molecules are responsible for the maintenance of airway obstruction in asthma. Moreover, there are systemic consequences of the inflammatory responses associated with COPD. For example, there is ample literature demonstrating the association of inflammatory mediators such as TNFa and IL- 6 (both markedly increased in COPD) with abnormalities in body composition, weight loss, peripheral muscle wasting and loss of performance, and functional status.27-29 Findings of increased muscle apoptosis and shifts in muscle fiber composition may be related to the systemic inflammatory processes
associated with COPD. Other manifestations of systemic inflammation in COPD include an increased prevalence of osteoporosis and central nervous system defects.30,31 Finally, there is a growing interest in the role of inflammation in coronary artery disease progression and its potential association with COPD and pulmonary inflammation.