Infection in the Pathogenesis and Course of Chronic Obstructive Pulmonary Disease

New molecular, cellular, and immunologic techniques used to study host–pathogen interactions have led to a reexamination of the role of infection in chronic obstructive pulmonary disease (COPD). There is now considerable evidence that infection plays a major role in the pathogenesis and clinical course of COPD. A vicious circle of infection and inflammation is thought to lead to exacerbations of the disease. New molecular, cellular, and immunologic techniques used to study host–pathogen interactions have led to a reexamination of the role of infection in chronic obstructive pulmonary disease (COPD). Considerable evidence suggests that a vicious circle of infection and inflammation leads to exacerbations of the disease. Historical Perspective In the 1950s and 1960s, according to a theory known as the British hypothesis, repeated airway infection and hypersecretion of mucus were thought to be the causes of chronic obstructive pulmonary disease (COPD). Subsequently, exposure to tobacco smoke was identified as the predominant cause. Researchers were still unable to relate the frequency of exacerbations — acute increases in the respiratory symptoms of COPD that require medical intervention — and hypersecretion of mucus to the progression of airflow obstruction. 1 Instead, the frequency of bacterial isolation from sputum was found to be similar in stable COPD and during exacerbations. On . . .