中华结核和呼吸杂志
中華結覈和呼吸雜誌
중화결핵화호흡잡지
Chinese Journal of Tuberculosis and Respiratory Diseases
2014年
12期
903-908
,共6页
老启芳%曾小良%钟小宁%张建全%何志义
老啟芳%曾小良%鐘小寧%張建全%何誌義
로계방%증소량%종소저%장건전%하지의
肺疾病,慢性阻塞性%吸烟%炎症
肺疾病,慢性阻塞性%吸煙%炎癥
폐질병,만성조새성%흡연%염증
Pulmonary disease,chronic obstructive%Smoking%Inflammation
目的 研究肺功能正常吸烟者和慢性阻塞性肺疾病(慢阻肺)患者肺腺泡动脉炎症与小气道炎症的相关性.方法 选取广西医科大学第一附属医院心胸外科因周围型肺癌行肺叶切除术的33例患者,其中男30例,女3例,年龄(61±9)岁,分为A组(肺功能正常不吸烟组,10例)、B组(肺功能正常吸烟组,13例)、C组(吸烟慢阻肺稳定期组,10例),取手术切除的远离肺癌病灶的正常肺组织,HE和维多利亚蓝+范吉逊染色检测各组肺腺泡肌型动脉(MA)及小气道病理形态改变,测量MA管壁厚度并计算小气道病理积分,使用免疫组织化学方法检测淋巴细胞在MA和小气道的浸润水平,并分析MA炎症和小气道炎症的相关性.结果 3组患者MA管壁厚度分别为(119±11)、(139±25)和(172 ±28)μm,小气道病理积分分别为(49±10)、(101±34)和(163 ±36)分,B组和C组均明显高于A组,且C组明显高于B组(均P ＜0.05).B组和C组CD3+总T细胞、CD8+ T细胞在MA内膜、中膜、外膜及小气道上皮层、固有层、外膜层浸润较A组均增加,以MA外膜及小气道外膜层CD8+T细胞浸润为明显(均P＜0.05);C组较A组CD4T细胞在小气道上皮层、固有层、外膜层表达也增高(均P＜0.05),气道壁全层CD4/CD8+降低(P＜0.01),而CD4+T细胞在3组MA各层比较差异均无统计学意义(均P ＞0.05);B淋巴细胞在3组MA及小气道各层比较差异均无统计学意义(均P ＞0.05).MA管壁CD3+总T细胞、CD8+T细胞浸润程度与小气道病理总积分呈正相关(r值分别为0.431、0.633,均P＜0.05);CD3+总T细胞、CD8+T细胞在MA管壁浸润程度与其在小气道壁的浸润程度呈正相关(r值分别为0.655、0.725,均P＜0.01);MA管壁及小气道壁CD8+T细胞浸润程度与MA管壁厚度呈正相关(r值分别为0.589、0.556,均P＜0.01).结论 肺功能正常吸烟者和慢阻肺患者肺动脉炎症和小气道炎症均是以管壁全层尤其是外膜为主,主要以CD8+T细胞浸润为特征的同一性质的炎症,且两者密切相关,是慢阻肺全肺炎症的一部分,共同促进慢阻肺的发展.
目的 研究肺功能正常吸煙者和慢性阻塞性肺疾病(慢阻肺)患者肺腺泡動脈炎癥與小氣道炎癥的相關性.方法 選取廣西醫科大學第一附屬醫院心胸外科因週圍型肺癌行肺葉切除術的33例患者,其中男30例,女3例,年齡(61±9)歲,分為A組(肺功能正常不吸煙組,10例)、B組(肺功能正常吸煙組,13例)、C組(吸煙慢阻肺穩定期組,10例),取手術切除的遠離肺癌病竈的正常肺組織,HE和維多利亞藍+範吉遜染色檢測各組肺腺泡肌型動脈(MA)及小氣道病理形態改變,測量MA管壁厚度併計算小氣道病理積分,使用免疫組織化學方法檢測淋巴細胞在MA和小氣道的浸潤水平,併分析MA炎癥和小氣道炎癥的相關性.結果 3組患者MA管壁厚度分彆為(119±11)、(139±25)和(172 ±28)μm,小氣道病理積分分彆為(49±10)、(101±34)和(163 ±36)分,B組和C組均明顯高于A組,且C組明顯高于B組(均P ＜0.05).B組和C組CD3+總T細胞、CD8+ T細胞在MA內膜、中膜、外膜及小氣道上皮層、固有層、外膜層浸潤較A組均增加,以MA外膜及小氣道外膜層CD8+T細胞浸潤為明顯(均P＜0.05);C組較A組CD4T細胞在小氣道上皮層、固有層、外膜層錶達也增高(均P＜0.05),氣道壁全層CD4/CD8+降低(P＜0.01),而CD4+T細胞在3組MA各層比較差異均無統計學意義(均P ＞0.05);B淋巴細胞在3組MA及小氣道各層比較差異均無統計學意義(均P ＞0.05).MA管壁CD3+總T細胞、CD8+T細胞浸潤程度與小氣道病理總積分呈正相關(r值分彆為0.431、0.633,均P＜0.05);CD3+總T細胞、CD8+T細胞在MA管壁浸潤程度與其在小氣道壁的浸潤程度呈正相關(r值分彆為0.655、0.725,均P＜0.01);MA管壁及小氣道壁CD8+T細胞浸潤程度與MA管壁厚度呈正相關(r值分彆為0.589、0.556,均P＜0.01).結論 肺功能正常吸煙者和慢阻肺患者肺動脈炎癥和小氣道炎癥均是以管壁全層尤其是外膜為主,主要以CD8+T細胞浸潤為特徵的同一性質的炎癥,且兩者密切相關,是慢阻肺全肺炎癥的一部分,共同促進慢阻肺的髮展.
목적 연구폐공능정상흡연자화만성조새성폐질병(만조폐)환자폐선포동맥염증여소기도염증적상관성.방법 선취엄서의과대학제일부속의원심흉외과인주위형폐암행폐협절제술적33례환자,기중남30례,녀3례,년령(61±9)세,분위A조(폐공능정상불흡연조,10례)、B조(폐공능정상흡연조,13례)、C조(흡연만조폐은정기조,10례),취수술절제적원리폐암병조적정상폐조직,HE화유다리아람+범길손염색검측각조폐선포기형동맥(MA)급소기도병리형태개변,측량MA관벽후도병계산소기도병리적분,사용면역조직화학방법검측림파세포재MA화소기도적침윤수평,병분석MA염증화소기도염증적상관성.결과 3조환자MA관벽후도분별위(119±11)、(139±25)화(172 ±28)μm,소기도병리적분분별위(49±10)、(101±34)화(163 ±36)분,B조화C조균명현고우A조,차C조명현고우B조(균P ＜0.05).B조화C조CD3+총T세포、CD8+ T세포재MA내막、중막、외막급소기도상피층、고유층、외막층침윤교A조균증가,이MA외막급소기도외막층CD8+T세포침윤위명현(균P＜0.05);C조교A조CD4T세포재소기도상피층、고유층、외막층표체야증고(균P＜0.05),기도벽전층CD4/CD8+강저(P＜0.01),이CD4+T세포재3조MA각층비교차이균무통계학의의(균P ＞0.05);B림파세포재3조MA급소기도각층비교차이균무통계학의의(균P ＞0.05).MA관벽CD3+총T세포、CD8+T세포침윤정도여소기도병리총적분정정상관(r치분별위0.431、0.633,균P＜0.05);CD3+총T세포、CD8+T세포재MA관벽침윤정도여기재소기도벽적침윤정도정정상관(r치분별위0.655、0.725,균P＜0.01);MA관벽급소기도벽CD8+T세포침윤정도여MA관벽후도정정상관(r치분별위0.589、0.556,균P＜0.01).결론 폐공능정상흡연자화만조폐환자폐동맥염증화소기도염증균시이관벽전층우기시외막위주,주요이CD8+T세포침윤위특정적동일성질적염증,차량자밀절상관,시만조폐전폐염증적일부분,공동촉진만조폐적발전.
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 CD3+ T-lymphocytes and CD8+ 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 CDs8+ T-lymphocytes infiltration in adventitia of MA and small airway (P ＜ 0.05).Expression of CD4+ 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 CD4+/CDs+ 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 CD3+ Tlymphocytes and CD8+ 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 CD3+ T-lymphocytes and CD8+ T-lymphocytes infiltration in MA showed positive correlation with that in small airway (r =0.655,0.725,P ＜ 0.01).The degree of CD8+ 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,CDs+ 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.
