Inflammation and Treatment in Asthma and COPD

By James F. Donohue, MD, FCCP; and Jill A. Ohar, MD, FCCP

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Asthma

Chronic Inflammation

The physiologic and clinical features of asthma derive from interactions among resident and infiltrating inflammatory cells and from the increased airway smooth muscle responsiveness caused by both bronchoconstriction and inflammation. The severity of asthma correlates with the extent of inflammation, sputum eosinophilia, and neutrophilia. The site of inflammation is primarily in peripheral airways, but the central airways, alveoli, and bronchiolar tissues are also inflamed. Inflammatory cells have prolonged survival in asthma, a phenomenon reversed by inhaled corticosteroids (ICSs). Neutrophils play an important role in patients with more severe, long-standing asthma. Irreversible airflow obstruction, also known as remodeling, develops in some patients with asthma, even those with mild disease. Although the pathophysiology and pathogenesis of this airway remodeling are not completely understood, it is likely caused by chronic airway inflammation. Recent evidence suggests that treatment with ICSs may prevent remodeling or control its intensity in some patients. In a study of patients with mild asthma, Olivieri and colleagues⁷ found that treatment with fluticasone significantly reduced the number of inflammatory cells as well as the inflammatory process, thereby modulating collagen deposition beneath the basement membrane. Although long-acting b₂-agonists are potent inhibitors of mast cells and reduce neovascularity, there is no evidence that they have anti-inflammatory effects or affect airway wall remodeling.

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