Mast cells in the airway lumen and bronchial mucosa of patients with chronic bronchitis.

Abstract

In order to evaluate the degree of mast cell infiltration and determine their granulation state in the airways of patients with chronic bronchitis, bronchoscopy was performed in 25 chronic bronchitis subjects (10 smokers and 15 ex-smokers) with mucoid sputum production and in seven normal nonsmoking control subjects. Bronchoalveolar lavage and bronchial biopsies were examined using histochemical techniques. Subjects with chronic bronchitis had higher numbers of mast cells both in the epithelium (1.22 +/- 1 versus 0.22 +/- 0.2 mast cells per mm) and in the bronchial glands (137.4 +/- 37.9 versus 38 +/- 5.1 mast cells per mm2) than did control subjects (p < 0.01 and p < 0.001, respectively), whereas the numbers of mast cells in bronchoalveolar lavage (0.21 +/- 0.1 versus 0.18 +/- 0.1 mast cells percentage, nonsignificant [NS]) and in the lamina propria (87.5 +/- 66.4 versus 87.2 +/- 61.8 mast cells per mm2, NS) were similar in the two groups. In the smoking group of bronchitics an increase in mast cell numbers was observed in epithelium (1.6 +/- 1.3 versus 0.95 +/- 0.7 mast cells per mm, NS), in lamina propria (112.2 +/- 86.5 versus 71.7 +/- 45.7 mast cells per mm2), and in BAL (0.26 +/- 0.21 versus 0.16 +/- 0.17 mast cell percentage of total cells, NS) in comparison with the ex-smoker's group of bronchitics.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers

“…This suggests an ongoing inflammatory process in the airways, in agreement with cross-sectional studies in smokers and exsmokers with COPD [3,4,9]. The presented sputum data also suggests that inflammation continues and even increases after smoking cessation.…”

“…Airway inflammation in bronchial biopsies and sputum did not differ between smokers and ex-smokers, except for some cytokines (interleukin (IL)-8, IL-6, soluble tumour necrosis factor-receptor (sTNF-R)75 and sTNF-R55) [3][4][5][6][7][8]. Furthermore, RUTGERS et al [9] showed that airway inflammation was more extensive in ex-smokers with COPD than in healthy ex-smokers.…”

Smoking cessation improves both direct and indirect airway hyperresponsiveness in COPD

“…The observed improvement in AHR to the indirect stimulus AMP after smoking cessation may result from a decreased number or activation state of mast cells in the airway wall. Indeed, PESCI et al [32] showed that the number of mast cells in bronchial epithelium, the lamina propria and bronchoalveolar lavage tended be lower in bronchial biopsies of exsmokers with COPD than in smokers with COPD. Mast cell numbers in sputum are far too low for useful determination, thus any evaluation of a possible contribution was impossible in the current study.…”

Association of current smoking with airway inflammation in chronic obstructive pulmonary disease and asymptomatic smokers

“…For example, higher numbers of CD8 positive T-cells, macrophages, neutrophils, and mast cells, both in central and peripheral airways have been found in COPD patients, irrespective whether these patients were current smokers or ex-smokers [4][5][6][7][8][9][10]. In addition, the percentage of neutrophils and IL-8 levels in sputum and broncho-alveolar lavage of COPD patients were higher [7,[11][12][13][14][15][16].…”