Nature of airway inflammation and remodeling in chronic cough

Chronic cough may be a result of asthma and nonasthma causes, but it is unclear whether there are specific inflammatory or remodeling changes. We determined airway mucosal changes in patients presenting with asthmatic cough and cough associated with nonasthmatic causes. Patients with chronic cough of nonasthmatic (n = 33; postnasal drip/rhinitis in 6, gastroesophageal reflux in 5, bronchiectasis in 3, and idiopathic in 19) and asthmatic (n = 14) causes and 15 healthy controls underwent fiberoptic bronchoscopy. Morphometry of bronchial biopsies and capsaicin cough sensitivity were assessed. Compared with controls, submucosal eosinophils and neutrophils were increased in patients with asthmatic cough ( P < .005) and submucosal mast cells in patients with nonasthmatic cough ( P = .01). Subbasement membrane thickness, goblet cell area, vascularity, and vessel size were also increased in both groups. Smooth muscle area was higher only in patients with nonasthmatic cough ( P = .0007 vs control and P = .019 vs asthmatic cough). None of the pathologic changes were related to the duration of coughing. Cough sensitivity was heightened in patients with nonasthmatic cough compared with controls and patients with asthmatic cough. The degree of goblet cell hyperplasia and epithelial shedding positively correlated with cough sensitivity in patients with nonasthmatic cough ( r = 0.43; P = .01; and r = 0.40; P = .02, respectively). Features of airway wall remodeling are prominent in the airways with nonasthmatic as well as asthmatic cough. These are linked to chronic cough rather than to asthma. Mast cell hyperplasia rather than eosinophilia is distinctive for nonasthmatic cough.