Purpose of review: Chronic obstructive pulmonary disease (COPD) is defined by airflow obstruction and is associated with an exaggerated inflammatory response to noxious stimuli, such as cigarette smoke. Inflammation and recruitment of immune cells drives the underlying pathophysiology; however, the roles of immune cells in the pathogenesis of COPD are evolving and this review will discuss the latest advancements in this field.
Recent findings: Leukocytes including macrophages, neutrophils and lymphocytes are increased in the airways of COPD patients. Despite the presence of increased innate immune cells, COPD airways are often colonized with bacteria suggesting an underlying defect. Macrophages from COPD patients have reduced phagocytic ability which may drive the persistence of inflammation. Differing macrophage phenotypes have been associated with disease suggesting that the surrounding pulmonary environment in COPD may generate a specific phenotype that is permanently pro-inflammatory. COPD neutrophils are also aberrant with increased survival and motility, but lack direction which could lead to more widespread destruction during migration. Finally, an element of autoimmunity, driven by Th17 cells, and alterations in the ratios of lymphocyte subsets may also be involved in disease progression.
Summary: COPD pathogenesis is complex with contributions from both the innate and adaptive immune systems, and the interaction of these cells with their environment mediates inflammation.