Source: Annual Congress 2003 - Respiratory structure and mechanisms: current concepts
Disease area: Airway diseases

Abstract

Cigarette smoking induces an airway inflammatory reaction, which may have direct effects on bronchiolar smooth muscle. As most of the inflammatory mediators are rapidly inactivated once they leave the cell, the microlocalization of inflammatory cells within the smooth muscle bundles may be crucial for their activity. To investigate the different cell types infiltrating airway smooth muscle in smokers, we analysed surgical specimens from 2 groups of subjects undergoing thoracotomy for localized pulmonary lesions: 20 smokers with a wide range of pulmonary function (range FEV₁:54-116% pred) and 9 nonsmokers with normal lung function (range FEV₁:92-148% pred). By immunohistochemistry we quantified the number of neutrophils, mast cells, macrophages, CD4 and CD8 T-cells within the smooth muscle of peripheral airways. Smokers had an increased number of neutrophils within airway smooth muscle compared to nonsmokers (38, 0-114 cells/mm² vs 6, 0-38 cells/mm²;p=0.002). When all subjects were considered together the number of neutrophils within airway smooth muscle showed a negative correlation with both the values of FEV₁ (% pred) (r = -0.45; p= 0.014) and FEV₁/FVC (%) (r = -0.035; p=0.05). The number of mast cells, macrophages, CD4 and CD8 T-cells was similar in the two groups of subjects examined. In conclusion, neutrophils are selectively recruited within the airway smooth muscle in smokers and may play a role in the development of functional abnormalities induced by cigarette smoking.

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S. Baraldo, C. Badin, R. Zuin, G. Turato, G. Casoni, B. Beghé, E. Balestro, A. Palamidese, P. Maestrelli, A. Papi, L. M. Fabbri, M. Saetta (Italy). Airway smooth muscle inflammation in smokers. Eur Respir J 2003; 22: Suppl. 45, 163

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