[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.

[The effect of moxifloxacin on apoptosis of airway smooth muscle cells and mitochondria membrane potential].

OBJECTIVE: To observe the effects of moxifloxacin at various concentrations on the expression of Caspase-3, the alteration of mitochondria membrane potential (ΔΨm) and the apoptosis of airway smooth muscle cells (ASMCs), and to explore the possible mechanisms. METHODS: ASMCs were derived from rat airway tissues and cultured in vitro. The cells were randomly divided into 5 groups including a control group and 4 groups to which moxifloxacin was added at different concentrations (40, 80, 120, 200 mg/L, groups M40, M80, M120 and M200 respectively). Then the cells of different groups were incubated for 48 h. An apoptosis detection kit was used for annexin V and PI staining, and JC-1 probe was employed to measure mitochondrial depolarization in ASMCs, and the protein of Caspase-3 was measured by Western blot. RESULTS: The apoptosis rates of ASMCs in groups M40, M80, M120 and M200 were (2.95 ± 0.21)%, (7.39 ± 0.63)%, (13.39 ± 0.40)% and (21.20 ± 1.42)%, respectively, all of which were higher than that in the control group (0.94 ± 0.05)%, F = 399.77, P < 0.01. Furthermore, the concentration of moxifloxacin was positively related to the apoptosis rate (r = 0.974, P < 0.01). Compared to the control group (the ratio of orange-red fluorescence to green fluorescence was 10.02 ± 0.20), there was a shift from mitochondrial orange-red fluorescence to green fluorescence among groups with the concentrations of moxifloxacin increasing (6.54 ± 0.15, 4.48 ± 0.14, 2.25 ± 0.10 and 1.99 ± 0.12); the difference was significant (F = 1565.12, P < 0.01), and there was a dose-dependent response (r = -0.946, P < 0.01). The results of Western blot indicated that the expression of Caspase-3 increased with the concentrations of moxifloxacin increasing (0.45 ± 0.05, 0.59 ± 0.04, 0.69 ± 0.06 and 0.84 ± 0.04, respectively), and there was a very low expression of Caspase-3 in the control group (0.31 ± 0.03). The expression of Caspase-3 showed a positive correlation with the concentration of moxifloxacin (r = 0.979, P < 0.01). The apoptosis rate of ASMCs in the different groups had a remarkable correlation with the ΔΨm and Caspase-3 (r = -0.887, P < 0.01; r = 0.955, P < 0.01). There was also a remarkable negative correlation between ΔΨm and Caspase-3 (r = -0.951, P < 0.01). CONCLUSION: Moxifloxacin was shown to promote ASMC apoptosis by altering ΔΨm.