CD8-LYMPHOCYTES IN PERIPHERAL AIRWAYS OF SMOKERS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE( T)

Citation
M. Saetta et al., CD8-LYMPHOCYTES IN PERIPHERAL AIRWAYS OF SMOKERS WITH CHRONIC OBSTRUCTIVE PULMONARY-DISEASE( T), American journal of respiratory and critical care medicine, 157(3), 1998, pp. 822-826
Citations number
33
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
157
Issue
3
Year of publication
1998
Pages
822 - 826
Database
ISI
SICI code
1073-449X(1998)157:3<822:CIPAOS>2.0.ZU;2-5
Abstract
To investigate whether the inflammatory process in peripheral airways is different in smokers who develop symptoms of chronic bronchitis and chronic airflow limitation and in asymptomatic smokers who do not dev elop chronic airflow limitation, we examined surgical specimens obtain ed from 16 smokers undergoing lung resection for localized pulmonary l esions. Nine had symptoms of chronic bronchitis and chronic airflow li mitation and seven were asymptomatic with normal lung function. In per ipheral airways, immunohistochemical methods were performed to identif y neutrophils, macrophages, CD4(+) and CD8(+) T-lymphocytes infiltrati ng the airway wall, and morphometric methods were used to measure the internal perimeter, the airway wall area, and the smooth muscle area. The number of CD8(+) T-lymphocytes and the smooth muscle area were inc reased in smokers with symptoms of chronic bronchitis and chronic airf low limitation as compared with asymptomatic smokers with normal lung function, while the number of neutrophils, macrophages, and CD4(+) T-l ymphocytes were similar in the two groups of subjects examined. We con cluded that smokers who develop symptoms of chronic bronchitis and chr onic airflow limitation have an increased number of CD8(+) T-lymphocyt es and an increased smooth muscle area in the peripheral airways as co mpared with asymptomatic smokers with normal lung function, supporting the important role of CD8(+) T-lymphocytes and airway remodeling in t he pathogenesis of chronic obstructive pulmonary disease.