Characteristics of the Inflammation in Biopsies from Large Airways of Subjects with Asthma and Subjects with Chronic Airflow Limitation

Abstract

Abstract Although the characteristics of the histopathologic changes present in subjects who die with status asthmaticus are well documented, the structural changes present in subjects with mild to moderately severe asthma are not well described and the inflammatory changes in the large airways of subjects with chronic airflow limitation (CAL) and asthma have not been compared. Ten subjects with asthma, five taking inhaled corticosteroids and five taking β2-agonist aerosols, five subjects with CAL, and four subjects with no respiratory illness had four biopsies taken from airways 10 mm in diameter. The length of intact epithelium, thickness of basement membrane, and number of lymphocytes, neutrophils, eosinophils, plasma cells, monocytes, and mast cells in the lamina propria, bronchial smooth muscle, and submucosa were measured. Intact epithelium was present along 56% of the basement membrane in the asthmatic subjects, along 54% in the subjects with CAL, and along 84% in the control subjects. In the asthmatic subjects there was no direct relationship between the severity of asthma and the amount of epithelial cell loss or the number of inflammatory cells. The basement membrane was thickened in all asthmatic subjects but not in normal subjects or subjects with CAL. There was a significant increase in the number of lymphocytes, eosinophils, and mast cells in the asthmatic airways, particularly in the lamina propria, compared with the CAL subjects. There were no eosinophils or mast cells in any of the control subjects. The airways of subjects with CAL contained significantly more inflammatory cells than the control subjects. Subjects with asthma on inhaled corticosteroids had significantly fewer lymphocytes, eosinophils, and mast cells compared with subjects taking only β2-agonists. There was very little variability in the amount of inflammation and the cells present between the four biopsies from each subject. We conclude that biopsies of large airways can be used to quantitate inflammation, and subjects with mild to moderately severe asthma have different inflammatory changes from subjects with CAL. There is no relationship between the severity of asthma, as measured by symptoms, bronchodilator use, and bronchial hyperresponsiveness, and the number of inflammatory cells present. However, the characteristics of the inflammation are different between subjects who are and are not taking inhaled corticosteroids.