Neutrophils infiltrating bronchial epithelium in chronic obstructive pulmonary disease

Abstract

In order to characterize neutrophil and eosinophil presence in the airways of patients with chronic obstructive pulmonary disease (COPD), bronchoscopy with bronchial washings and bronchial biopsies was performed in 12 smoking stable COPD subjects and 18 normal non-smoking control subjects. Bronchial biopsies were examined by light microscopy using plastic embedding and histochemical techniques to identify different cell types. Bronchial washing fluid of COPD patients was characterized by a predominance of neutrophils (P = 0.001), and a slight, but significant (P = 0.03), increase of eosinophil fraction. Subjects with COPD had higher number of neutrophils in the epithelium (P = 0.01), and eosinophils in the lamina propria (P = 0.01) than did control subjects. The thickness of reticular basement membrane was increased for COPD patients in comparison to control subjects (P = 0.01). The present study provides evidence of neutrophil infiltration both in bronchial washing and bronchial epithelium of patients with COPD, suggesting that the source of neutrophils in airway lumen may be the bronchial mucosa. Although less common than in asthma, airways of COPD subjects reveal eosinophil presence and airway remodelling.

Reticular basement membrane in asthma and COPD: Similar thickness, yet different composition

“…RBM thickness and composition in asthma and COPD status. 1,5,7,[9][10][11][12][13]15,17,22, Taken together, we conclude that an increased RBM thickness indicates the presence of asthma or COPD, irrespective of age and that it is not possible to differentiate mild-to-moderate asthma from COPD purely based on RBM thickness. In addition, a normal RBM thickness does not exclude obstructive airway disease.…”

“…Some studies fi nd a normal RBM, [6][7][8] while others report it to be thickened, [9][10][11][12][13] but generally to a smaller extent than in asthma. 9,10,12,14,15 The differences in observations may be due to the fact that some studies have included only a few COPD patients 7 or COPD patients with only mild 10 or more severe 9 airway obstruction.…”

“…9,10,12,14,15 The differences in observations may be due to the fact that some studies have included only a few COPD patients 7 or COPD patients with only mild 10 or more severe 9 airway obstruction. In addition, some studies included healthy controls who were either never smokers 11 or smokers not being matched for pack-years smoking. 8 Airway infl ammation is of a chronic nature in both asthma and COPD, likely resulting in a long-lasting increase of fi brogenic growth factors like transforming growth factor-β in both asthma and COPD, 10,16 vascular endothelial growth factor in asthma, 17 and epidermal growth factors in COPD.…”

Subepithelial immunopathology of the large airways in smokers with and without chronic obstructive pulmonary disease

“…The discordance of these results with those showing an increase in numbers of neutrophils and markers of neutrophil activation in bronchoalveolar lavage [10,11,13,14,25], induced sputum [26±28] and airway epithelium [29] remains to be explained.…”

A mouse GM-CSF receptor antibody attenuates neutrophilia in mice exposed to cigarette smoke

“…COPD is characterised by irreversible airflow obstruction and progressive lung inflammation that correlates with disease severity [2]. Whilst asthma is more associated with eosinophilic inflammation, in COPD, neutrophils and macrophages predominate [3].…”