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  • Title: [The relationship between pulmonary arterial and small airway inflammation in smokers with and without chronic obstructive pulmonary disease].
    Author: Lao Q, Zeng X, Zhong X, Zhang J, He Z.
    Journal: Zhonghua Jie He He Hu Xi Za Zhi; 2014 Dec; 37(12):903-8. PubMed ID: 25609127.
    Abstract:
    OBJECTIVE: To investigate the relationship between pulmonary arterial and small airway inflammation in smokers with normal lung function and smokers with chronic obstructive pulmonary disease (COPD). METHODS: Patients requiring lung resection for peripheral lung cancer were divided into group A (nonsmokers with normal lung function, n = 10), group B (smokers with normal lung function, n = 13) and group C (smokers with stable COPD, n = 10). Normal pulmonary tissue was obtained more than 5 cm away from cancer lesion. The pathomorphological changes of the pulmonary muscularized arteries (MA) and small airways were observed by HE and Victoria blue-Van Gieson's stains.Lymphocytes infiltrated in the MA and small airways were observed by immunohistochemical methods. The characteristics and the correlations between pulmonary arterial inflammation and small airway inflammation were analyzed. RESULTS: The thickness of MA wall in the three groups was (119 ± 11), (139 ± 25) and (172 ± 28) µm respectively. The total small airway pathology score was (49 ± 10), (101 ± 34) and (163 ± 36) respectively. The score in group B and C was significantly higher than that in group A (P < 0.05), and the thickness of MA wall and total small airway pathology score in group C was significantly higher than that in group B (P < 0.05). The degree of CD(+)(3) T-lymphocytes and CD(+)(8) T-lymphocytes infiltration in the intima, media and adventitia of MA and epithelial layer, lamina propria and adventitia of small airway in group B and C was more significant than that in group A, especially CD(+)(8) T-lymphocytes infiltration in adventitia of MA and small airway (P < 0.05). Expression of CD(+)(4) T-lymphocytes on epithelial layer, lamina propria and adventitia of small airway in group C was higher than that in group A (P < 0.05), but the CD(+)(4)/CD(+)(8) ratio in the whole layer of airway wall declined (P < 0.01). Among three groups, the infiltration of B-lymphocytes in three layers compared each other had no statistical differences (P > 0.05). The infiltration of CD(+)(3)T-lymphocytes and CD(+)(8)T-lymphocytes in the whole layer of MA was positively correlated with the total small airway pathology score respectively (r = 0.431,0.633, P < 0.05), and the degree of CD(+)(3)T-lymphocytes and CD(+)(8)T-lymphocytes infiltration in MA showed positive correlation with that in small airway (r = 0.655,0.725, P < 0.01). The degree of CD(+)(8)T-lymphocytes infiltration in MA and small airway was positively correlated with thickness of MA (r = 0.589,0.556, P < 0.01). CONCLUSIONS: Both in smokers with normal lung function and smokers with stable COPD, CD(+)(8)T-lymphocytes infiltration in the whole layer of pulmonary arteries and small airways is the same kind of inflammation, mainly in the adventitia of pulmonary arteries and small airways. They are a part of pulmonary inflammation in COPD and promote the development of COPD.
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