CAJ | 학술논문

目的探讨游离免疫球蛋白轻链(FLC)在吸烟肺功能正常者和慢性阻塞性肺疾病(简称慢阻肺)患者肺部炎症机制中的作用及临床意义.方法收集徐州医学院附属医院胸外科2012年8-12月因周围型肺癌行肺叶切除术患者32例,分为3组.不吸烟肺功能正常组(不吸烟组)10例,吸烟肺功能正常组(吸烟组)12例,吸烟慢阻肺稳定期组(慢阻肺组)10例.取术前清晨空腹血清及癌旁肺组织,酶联免疫吸附试验(ELISA)检测血清和肺组织匀浆中FLC-λ和FLC-κ含量,免疫组织化学法检测FLC-λ和FLC-κ在气道上皮、肺泡壁和血管壁的表达,分析FLC表达与肺功能指标的相关关系.结果慢阻肺组、吸烟组血清FLC-λ和FLC-κ含量分别为(35 ±11)、(38±12)和(26 ±9)、(26 ±8) mg/L,均显著高于不吸烟组[(16±7)和(16±5) mg/L],差异均有统计学意义(q值分别为3.590 ～7.482,P＜0.01);慢阻肺组显著高于吸烟组(q值分别为3.209～ 4.198,P＜0.05和P＜0.01).慢阻肺组和吸烟组肺组织匀浆中FLC-λ和FLC-κ含量分别为(1.29±0.31)、(1.32±0.30)和(0.86±0.42)、(0.85±0.37)μg/mg,均显著高于不吸烟组[(0.45±0.18)和(0.42±0.13) μg/mg],差异均有统计学意义(q值分别为4.178～9.795,P＜0.05和P＜0.01);慢阻肺组显著高于吸烟组(q值分别为4.269 ～4.349,均P＜0.05).在气道上皮、肺泡壁和血管壁中均有FLC-λ和FLC-κ表达.血清和肺组织匀浆中FLC-λ和FLC-κ含量与FEV1占预计值％均呈显著负相关(r值为-0.476 ～-0.591,均P＜0.01).结论慢阻肺患者和吸烟肺功能正常者血清和肺组织中FLC表达增加,与气流受限密切相关,提示FLC在慢阻肺患者和吸烟者肺部炎症反应发生机制中有促炎作用.
목적 탐토유리면역구단백경련(FLC)재흡연폐공능정상자화만성조새성폐질병(간칭만조폐)환자폐부염증궤제중적작용급림상의의.방법 수집서주의학원부속의원흉외과2012년8-12월인주위형폐암행폐협절제술환자32례,분위3조.불흡연폐공능정상조(불흡연조)10례,흡연폐공능정상조(흡연조)12례,흡연만조폐은정기조(만조폐조)10례.취술전청신공복혈청급암방폐조직,매련면역흡부시험(ELISA)검측혈청화폐조직균장중FLC-λ화FLC-κ함량,면역조직화학법검측FLC-λ화FLC-κ재기도상피、폐포벽화혈관벽적표체,분석FLC표체여폐공능지표적상관관계.결과 만조폐조、흡연조혈청FLC-λ화FLC-κ함량분별위(35 ±11)、(38±12)화(26 ±9)、(26 ±8) mg/L,균현저고우불흡연조[(16±7)화(16±5) mg/L],차이균유통계학의의(q치분별위3.590 ～7.482,P＜0.01);만조폐조현저고우흡연조(q치분별위3.209～ 4.198,P＜0.05화P＜0.01).만조폐조화흡연조폐조직균장중FLC-λ화FLC-κ함량분별위(1.29±0.31)、(1.32±0.30)화(0.86±0.42)、(0.85±0.37)μg/mg,균현저고우불흡연조[(0.45±0.18)화(0.42±0.13) μg/mg],차이균유통계학의의(q치분별위4.178～9.795,P＜0.05화P＜0.01);만조폐조현저고우흡연조(q치분별위4.269 ～4.349,균P＜0.05).재기도상피、폐포벽화혈관벽중균유FLC-λ화FLC-κ표체.혈청화폐조직균장중FLC-λ화FLC-κ함량여FEV1점예계치％균정현저부상관(r치위-0.476 ～-0.591,균P＜0.01).결론 만조폐환자화흡연폐공능정상자혈청화폐조직중FLC표체증가,여기류수한밀절상관,제시FLC재만조폐환자화흡연자폐부염증반응발생궤제중유촉염작용.
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.