中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2010年
20期
1431-1436
,共6页
张建全%老启芳%褚淑媛%白晶%钟小宁
張建全%老啟芳%褚淑媛%白晶%鐘小寧
장건전%로계방%저숙원%백정%종소저
白细胞介素17%肺疾病%慢性阻塞性%吸烟%炎症
白細胞介素17%肺疾病%慢性阻塞性%吸煙%炎癥
백세포개소17%폐질병%만성조새성%흡연%염증
Interleukin-17%Pulmonary disease,chronic obstructive%Smoking%Inflammation
目的 探讨白细胞介素17(IL-17)在肺功能正常吸烟者和慢性阻塞性肺疾病(COPD)患者肺部炎症反应发生机制中的作用.方法 将需手术治疗的周围型肺癌患者分为肺功能正常非吸烟组(NS组,10例)、肺功能正常吸烟组(S组,13例)和吸烟COPD稳定期组(COPD组,10例).于手术切除标本选取距肺癌病灶5 cm以上的新鲜正常肺组织,酶联免疫吸附试验检测各组肺组织匀浆IL-17含量,HE和维多利亚蓝+范吉逊染色检测各组平均肺泡面积、小气道病理总积分和肺腺泡肌型动脉(MA)管壁厚度,免疫组织化学方法检测IL-17+及CD4+、CD8+T细胞在肺泡壁、小气道壁及MA管壁的表达,分析IL-17表达与CD4+、CD8+T细胞以及与肺实质病理改变和肺功能指标的相关关系.结果 NS组、S组和COPD组肺组织匀浆IL-17含量分别为6.1(3.7～12.4)、9.7(3.5～69.7)和22.7(7.0～114.4)pg/mg,S组和COPD组明显高于明显NS组(P<0.05,P<0.01),COPD组明显高于S组(P<0.05);平均肺泡面积分别为(50 708±4 125)、(106 517±13 851)和(152 344±43 783)μm2,小气道病理总积分分别为(49±10)、(101±34)和(163±36)分,MA管壁厚度分别为(119±11)、(139±25)和(172±28)μm,S组和COPD组均明显高于NS组(P<0.05,P<0.01),COPD组明显高于S组(P<0.05,P<0.01).IL-17主要表达于肺实质浸润的炎症细胞,S组和COPD组肺泡壁、小气道壁及MA管壁IL-17+T细胞均明显多于NS组(均P<0.01),COPD组明显多于S组(均P<0.05).IL-17表达与平均肺泡面积(r=0.561)、小气道病理总积分(r=0.425)、MA管壁厚度(r=0.682)呈显著正相关(均P<0.05).肺泡壁、小气道壁和MA管壁中IL-17表达与CIM+、CD8+细胞呈显著正相关(P<0.05,P<0.01).肺组织匀浆IL-17含量与第1秒用力呼气容积占预计值百分比呈显著负相关(r=-0.471,P<0.01).结论 lL-17在肺功能正常吸烟者和COPD患者肺组织中表达增高,与肺CIM+、CD8+T细胞及肺组织破坏、气道炎症、肺动脉重构和气流受限密切相关,提示IL-17在吸烟者和COPD患者肺部炎症反应发生机制中有促炎作用.
目的 探討白細胞介素17(IL-17)在肺功能正常吸煙者和慢性阻塞性肺疾病(COPD)患者肺部炎癥反應髮生機製中的作用.方法 將需手術治療的週圍型肺癌患者分為肺功能正常非吸煙組(NS組,10例)、肺功能正常吸煙組(S組,13例)和吸煙COPD穩定期組(COPD組,10例).于手術切除標本選取距肺癌病竈5 cm以上的新鮮正常肺組織,酶聯免疫吸附試驗檢測各組肺組織勻漿IL-17含量,HE和維多利亞藍+範吉遜染色檢測各組平均肺泡麵積、小氣道病理總積分和肺腺泡肌型動脈(MA)管壁厚度,免疫組織化學方法檢測IL-17+及CD4+、CD8+T細胞在肺泡壁、小氣道壁及MA管壁的錶達,分析IL-17錶達與CD4+、CD8+T細胞以及與肺實質病理改變和肺功能指標的相關關繫.結果 NS組、S組和COPD組肺組織勻漿IL-17含量分彆為6.1(3.7～12.4)、9.7(3.5～69.7)和22.7(7.0～114.4)pg/mg,S組和COPD組明顯高于明顯NS組(P<0.05,P<0.01),COPD組明顯高于S組(P<0.05);平均肺泡麵積分彆為(50 708±4 125)、(106 517±13 851)和(152 344±43 783)μm2,小氣道病理總積分分彆為(49±10)、(101±34)和(163±36)分,MA管壁厚度分彆為(119±11)、(139±25)和(172±28)μm,S組和COPD組均明顯高于NS組(P<0.05,P<0.01),COPD組明顯高于S組(P<0.05,P<0.01).IL-17主要錶達于肺實質浸潤的炎癥細胞,S組和COPD組肺泡壁、小氣道壁及MA管壁IL-17+T細胞均明顯多于NS組(均P<0.01),COPD組明顯多于S組(均P<0.05).IL-17錶達與平均肺泡麵積(r=0.561)、小氣道病理總積分(r=0.425)、MA管壁厚度(r=0.682)呈顯著正相關(均P<0.05).肺泡壁、小氣道壁和MA管壁中IL-17錶達與CIM+、CD8+細胞呈顯著正相關(P<0.05,P<0.01).肺組織勻漿IL-17含量與第1秒用力呼氣容積佔預計值百分比呈顯著負相關(r=-0.471,P<0.01).結論 lL-17在肺功能正常吸煙者和COPD患者肺組織中錶達增高,與肺CIM+、CD8+T細胞及肺組織破壞、氣道炎癥、肺動脈重構和氣流受限密切相關,提示IL-17在吸煙者和COPD患者肺部炎癥反應髮生機製中有促炎作用.
목적 탐토백세포개소17(IL-17)재폐공능정상흡연자화만성조새성폐질병(COPD)환자폐부염증반응발생궤제중적작용.방법 장수수술치료적주위형폐암환자분위폐공능정상비흡연조(NS조,10례)、폐공능정상흡연조(S조,13례)화흡연COPD은정기조(COPD조,10례).우수술절제표본선취거폐암병조5 cm이상적신선정상폐조직,매련면역흡부시험검측각조폐조직균장IL-17함량,HE화유다리아람+범길손염색검측각조평균폐포면적、소기도병리총적분화폐선포기형동맥(MA)관벽후도,면역조직화학방법검측IL-17+급CD4+、CD8+T세포재폐포벽、소기도벽급MA관벽적표체,분석IL-17표체여CD4+、CD8+T세포이급여폐실질병리개변화폐공능지표적상관관계.결과 NS조、S조화COPD조폐조직균장IL-17함량분별위6.1(3.7～12.4)、9.7(3.5～69.7)화22.7(7.0～114.4)pg/mg,S조화COPD조명현고우명현NS조(P<0.05,P<0.01),COPD조명현고우S조(P<0.05);평균폐포면적분별위(50 708±4 125)、(106 517±13 851)화(152 344±43 783)μm2,소기도병리총적분분별위(49±10)、(101±34)화(163±36)분,MA관벽후도분별위(119±11)、(139±25)화(172±28)μm,S조화COPD조균명현고우NS조(P<0.05,P<0.01),COPD조명현고우S조(P<0.05,P<0.01).IL-17주요표체우폐실질침윤적염증세포,S조화COPD조폐포벽、소기도벽급MA관벽IL-17+T세포균명현다우NS조(균P<0.01),COPD조명현다우S조(균P<0.05).IL-17표체여평균폐포면적(r=0.561)、소기도병리총적분(r=0.425)、MA관벽후도(r=0.682)정현저정상관(균P<0.05).폐포벽、소기도벽화MA관벽중IL-17표체여CIM+、CD8+세포정현저정상관(P<0.05,P<0.01).폐조직균장IL-17함량여제1초용력호기용적점예계치백분비정현저부상관(r=-0.471,P<0.01).결론 lL-17재폐공능정상흡연자화COPD환자폐조직중표체증고,여폐CIM+、CD8+T세포급폐조직파배、기도염증、폐동맥중구화기류수한밀절상관,제시IL-17재흡연자화COPD환자폐부염증반응발생궤제중유촉염작용.
Objective To study the effect of interleukin 17 (IL-17) with mechanism of pulmonary inflammatory in smokers with normal lung junction and chronic obstructive pulmonary disease ( COPD) patients. Methods The peripheral lung cancer patients in need of a surgical therapy were divided into normal lung function and non-smoking group (NS group,n=10), normal lung function and smoking group (S group,n=13) and smoking with stable COPD group (COPD group,n=10). The fresh normal lung tissue was harvested from the surgical specimens with a margin of 5 cm away from resection foci. Then the lung tissue levels of IL-17 were detected with enzyme-linked immunosorbent assay. The average alveolar area, the total small airway pathology score and the pulmonary muscular artery (MA) wall thickness were measured by HE and Victoria blue-Van Gieson's stains. The IL-17+cells and CD4+, CD8+lymphocytes in alveolar walls, small airways and lung MA were analyzed by immunohistochemistry. The investigators also explored the relationships between IL-17 level, pathological morphology of pulmonary parenchyma, small airway, pulmonary artery reconstruction and pulmonary functions. Results The IL-17 levels in lung tissue of NS, S and COPD groups were 6. 1 (3.7-12.4), 9.7 (3.5-69.7) and 22.7 (7.0-114.4) pg/mg respectively. The S and COPD groups were significantly higher than the NS group (P < 0. 05, P < 0.01). The S group was significantly higher than the NS group (P<0. 05 ) . The average alveolar area were (50 708 ± 14 125), (106 517 ± 13 851) and (152 344 ± 43 783 )μm2 , the total small airway pathology score (49 ± 10) , (101 ±34) and (163 ±36), and the MA wall thickness (119 ± 11), (139 ± 25) and (172 ± 28) μm respectively. The S and COPD groups were significantly higher than the NS group ( P < 0. 05, P < 0. 01). And the COPD group was significantly higher than the S group (P < 0. 05, P < 0. 01). IL-17 was predominantly expressed in lung infiltration of inflammatory cells. IL-17 of alveolar walls, small airway wall and MA wall in the S and COPD groups were significantly higher than the NS group. And the COPD group was significantly higher than NS group (P < 0. 05). IL-17 + cells were positively correlated with the average alveolar area in pulmonary parenchyma (r = 0. 561, P < 0. 01), the pulmonary artery wall thickness in M A ( r =0. 682, P < 0. 01) and the pathological score in small airways (r =0. 425, P < 0. 05). IL-17 + cells of pulmonary parenchyma, small airways and MA were positively correlated with CD4 + and CD8 + lymphocytes in lung (P < 0. 05, P < 0.01). The levels of IL-17 in lung homogenate tissue showed a negative correlation with the FEV1 percentage of predicted value ( r = - 0. 471, P < 0. 01). Conclusions IL-17 is up-regulated in lung tissues of normal lung function smokers and COPD patients. And it has a close correlation with CD4 + and CD8 + lymphocytes in lung, lung parenchyma destruction, pulmonary inflammation, pulmonary artery reconstruction and airflow limitation. All of these suggest that IL-17 plays an important pro-inflammatory role in COPD.
