Airway inflammation in chronic obstructive pulmonary disease

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Airway inflammation in chronic obstructive pulmonary disease E.Rand Sutherland, MD, MPH, Richard J Martin, MD Journal of Allergy and Clinical Immunology Volume 112, Issue 5, Pages 819-827 (November 2003) DOI: 10.1016/S0091-6749(03)02011-6

FIG 1 In COPD cigarette smoking initiates a series of inflammatory events that lead to emphysema (top circle) and airway inflammation with epithelial damage and mucus hypersecretion (middle circle), both of which combine to cause the hallmark physiologic abnormality of expiratory airflow limitation (red flow-volume loop, bottom circle) Journal of Allergy and Clinical Immunology 2003 112, 819-827DOI: (10.1016/S0091-6749(03)02011-6)

FIG 2 Inverse correlation between CD8+ cells per cubic millimeter and FEV1 percent predicted in the central24 (left) and peripheral14 (right) airways of subjects with COPD. Journal of Allergy and Clinical Immunology 2003 112, 819-827DOI: (10.1016/S0091-6749(03)02011-6)

FIG 3 Increased peripheral airways resistance in patients with asthma. Reprinted with permission from Wagner et al. Journal of Allergy and Clinical Immunology 2003 112, 819-827DOI: (10.1016/S0091-6749(03)02011-6)

FIG 4 Pathologic changes in the airways of patients with COPD (top and bottom left) and asthma (top and bottom right). Immunostaining for eosinophils (EG2+) demonstrates subepithelial infiltration with these cells in asthma (top right) that is not seen in COPD (top left). Additionally, the reticular layer of the basement membrane is thicker in patients with asthma (bottom right) than in patients with COPD. Reprinted with permission. Journal of Allergy and Clinical Immunology 2003 112, 819-827DOI: (10.1016/S0091-6749(03)02011-6)