[Expression and significance of hypoxia-inducible factor-1α in patients with chronic obstructive pulmonary disease and smokers with normal lung function].

OBJECTIVE: To study the expression of hypoxia-inducible factor (HIF)-1α in lung tissues and sera from chronic obstructive pulmonary disease (COPD) patients and smokers with normal lung function and explore its clinical significance. METHODS: Lung tissue samples were obtained from 32 patients undergoing surgery for peripheral lung tumors. Lung function test was performed before lung cancer surgery. Based on lung function and smoking status, 32 patients were devided into three groups: smokers with stable COPD (COPD group, n=10), smokers with normal lung function (S group, n=10) and nonsmokers with nomal lung function (NS group, n=10). The preoperative fasting sera and lung tissues as far as possible away from the tumor site from all patients were collected. HIF-1α levels in sera and lung tissue homogenates were evaluated by ELISA. The expression of HIF-1α in airway epithelium, alveolar wall and blood vessel wall were detected by immunohistochemistry. Furthermore, the correlation between HIF-1α expression levels and pulmonary function was analyzed. RESULTS: Serum HIF-1α levels were significantly elevated in COPD group [(73.25 ± 6.12) pg/mL] and S group [(60.30 ± 8.00) pg/mL] as compared with NS group [(47.03 ± 8.43) pg/mL, P<0.01], and COPD group was significantly higher than S group (P<0.01). The concentrations of HIF-1α in lung tissue homogenates significantly increased in COPD group [(2.04 ± 0.24) pg/µg] and S group [(1.67 ± 0.34) pg/µg] as compared with NS group [(1.12 ± 0.33) pg/µg, P<0.01], and COPD group was also significantly higher than S group (P<0.01). HIF-1α expression was located in inflammatory cells and macrophages of airway epithelium, alveolar wall and small pulmonary artery wall. HIF-1α levels in sera and lung tissue homogenates showed negative correlations with FEV1/FVC and FEV1% predicted. CONCLUSION: HIF-1α levels are raised in sera and lung tissues of COPD patients and smokers with normal lung function, and they were positively correlated with the severity of airflow limitation.

[Expression and significance of immunoglobulin free light chains in serum and lung tissues from patients with chronic obstructive pulmonary disease].

OBJECTIVE: To study the association of free immunoglobulin light chain (FLC) with clinical manifestations and lung inflammation in smokers with normal lung function and chronic obstructive pulmonary disease (COPD) patients. METHODS: Thirty-two patients with peripheral lung cancer undergoing surgical resection were enrolled from the Department of Thoracic Surgery,Affiliated Hospital of Xuzhou Medical College. They were divided into non-smoking with normal lung function group (non-smoking group, 10 cases), smoking with normal lung function group (smoking group, 12 cases) and smoking with stable COPD group (COPD group, 10 cases). Their preoperative fasting serum and lung tissues away from cancer were used in the study.Enzyme-linked immunesorbent assays (ELISA) were used to detect the levels of FLC-λ and FLC-κ in serum and lung tissue homogenates. The expression of FLC-λ and FLC-κ in the airway epithelium, alveolar wall and blood vessel wall was detected by immunohistochemistry. The correlation between FLC levels and pulmonary functions were analyzed. RESULTS: The serum levels of FLC-λ and FLC-κ in COPD group and smoking group were (35 ± 11),(38 ± 12) and (26 ± 9),(26 ± 8) mg/L, respectively. They were all significantly increased compared with the non-smoking group [(16 ± 7),(16 ± 5) mg/L]. The differences were all statistically significant (q = 3.590-7.482, P < 0.01), and those of the COPD group were significantly higher than those of the smoking group (q = 3.209-4.198, P < 0.05 and P < 0.01). The concentrations of FLC-λ and FLC-κ in lung tissue homogenates of the COPD group and the smoking group were (1.29 ± 0.31),(1.32 ± 0.30) and (0.86 ± 0.42),(0.85 ± 0.37) µg/mg, respectively. They were all significantly increased compared with those of the non-smoking group [(0.45 ± 0.18),(0.42 ± 0.13) µg/mg],(q = 4.178- 9.795, P < 0.05 and P < 0.01). The levels of FLC-λ and FLC-κ in the lung tissue homogenates from the COPD group were significantly higher than those from the smoking group (q = 4.269-4.349, all P < 0.05). The expression of FLC-λ and FLC-κ was detected in airway epithelium, alveolar wall and blood vessel wall. The levels of FLC-λ and FLC-κ in serum and lung tissue homogenates showed a negative correlation with FEV1 percentage of predicted value (r = -0.476 to -0.591, all P < 0.01). CONCLUSIONS: Expressions of FLC were increased in the serum and the lung tissues of COPD patients and smokers with normal lung function, and closely correlated with airflow limitation. The results suggest that FLC plays a proinflammatory role in the pathogenesis of COPD.