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
2011年
8期
609-613
,共5页
龙翔%宋卫东%刘媛媛%徐平%丘韶校%张宁
龍翔%宋衛東%劉媛媛%徐平%丘韶校%張寧
룡상%송위동%류원원%서평%구소교%장저
肺疾病,慢性阻塞性%烟草烟污染%树突细胞
肺疾病,慢性阻塞性%煙草煙汙染%樹突細胞
폐질병,만성조새성%연초연오염%수돌세포
Pulmonary disease,chronic obstructive%Tobacco smoke pollution%Dendritic cells
目的 观察香烟烟雾暴露对大鼠肺组织树突细胞数量、成熟度及肺组织慢性炎症变化的影响.方法 将30只雄性F344大鼠按随机数字表法分为香烟烟雾暴露组(暴露组)、断烟组和健康对照组(对照组),每组10只.采用香烟烟雾暴露法建立大鼠COPD模型,HE染色法检测大鼠气道炎症病理评分及肺泡平均内衬间隔,免疫组织化学ABC法观察大鼠肺组织中CD11c+、CD86+和CD8+ T细胞的分布及数量变化,流式细胞术检测CD11c+/CD86+和CD11c+/主要组织相容性复合体(MHC)Ⅱ+与CD11c+树突细胞比值.结果 暴露组和断烟组大鼠肺组织中出现COPD特征性病理改变,气道炎症病理评分[(390±33)分和(324±28)分]及肺泡平均内衬间隔[(68±11)μm和(58±9)μm]明显高于对照组[(56±13)分和(36±6)μm],差异均有统计学意义(F值分别为459.85和34.03,均P＜0.05).暴露组和断烟组大鼠CD11c+树突细胞阳性率[(1.47±0.12)%和(1.30±0.17)%]及CD86+树突细胞阳性率[(1.26±0.18)%和(1.02±0.08)%]均明显高于对照组[(0.96±0.08)%和(0.65±0.03)%],差异均有统计学意义(F值分别为6.55和30.26,均P＜0.05);暴露组和断烟组大鼠CD8+T细胞阳性率[(2.72±0.15)%和(2.35±0.23)%]均明显高于对照组[(1.39±0.11)%],差异有统计学意义(F=16.07,P＜0.05);暴露组和断烟组大鼠CD11c+/CD86+树突细胞及CD11c+/MHCⅡ+树突细胞占CD11c+树突细胞比例[(5.5±0.4)%和(4.8±0.4)%]及[(4.2±0.3)%和(3.3±0.3)%]明显低于对照组[(8.0±0.5)%和(6.1±0.5)%],差异均有统计学意义(F值分别为14.34和12.82,均P＜0.05).暴露组与断烟组上述各项指标比较,差异均无统计学意义(t值为1.10～2.11,均P＞0.05).结论 香烟烟雾暴露诱导COPD大鼠肺组织中树突细胞数量明显增加,成熟度明显下降,断烟后此趋势无明显变化,且以CD8+ T细胞浸润为主的慢性炎症反应持续存在,提示树突细胞数量变化及成熟异常可能参与了COPD慢性炎症迁延进展.
目的 觀察香煙煙霧暴露對大鼠肺組織樹突細胞數量、成熟度及肺組織慢性炎癥變化的影響.方法 將30隻雄性F344大鼠按隨機數字錶法分為香煙煙霧暴露組(暴露組)、斷煙組和健康對照組(對照組),每組10隻.採用香煙煙霧暴露法建立大鼠COPD模型,HE染色法檢測大鼠氣道炎癥病理評分及肺泡平均內襯間隔,免疫組織化學ABC法觀察大鼠肺組織中CD11c+、CD86+和CD8+ T細胞的分佈及數量變化,流式細胞術檢測CD11c+/CD86+和CD11c+/主要組織相容性複閤體(MHC)Ⅱ+與CD11c+樹突細胞比值.結果 暴露組和斷煙組大鼠肺組織中齣現COPD特徵性病理改變,氣道炎癥病理評分[(390±33)分和(324±28)分]及肺泡平均內襯間隔[(68±11)μm和(58±9)μm]明顯高于對照組[(56±13)分和(36±6)μm],差異均有統計學意義(F值分彆為459.85和34.03,均P＜0.05).暴露組和斷煙組大鼠CD11c+樹突細胞暘性率[(1.47±0.12)%和(1.30±0.17)%]及CD86+樹突細胞暘性率[(1.26±0.18)%和(1.02±0.08)%]均明顯高于對照組[(0.96±0.08)%和(0.65±0.03)%],差異均有統計學意義(F值分彆為6.55和30.26,均P＜0.05);暴露組和斷煙組大鼠CD8+T細胞暘性率[(2.72±0.15)%和(2.35±0.23)%]均明顯高于對照組[(1.39±0.11)%],差異有統計學意義(F=16.07,P＜0.05);暴露組和斷煙組大鼠CD11c+/CD86+樹突細胞及CD11c+/MHCⅡ+樹突細胞佔CD11c+樹突細胞比例[(5.5±0.4)%和(4.8±0.4)%]及[(4.2±0.3)%和(3.3±0.3)%]明顯低于對照組[(8.0±0.5)%和(6.1±0.5)%],差異均有統計學意義(F值分彆為14.34和12.82,均P＜0.05).暴露組與斷煙組上述各項指標比較,差異均無統計學意義(t值為1.10～2.11,均P＞0.05).結論 香煙煙霧暴露誘導COPD大鼠肺組織中樹突細胞數量明顯增加,成熟度明顯下降,斷煙後此趨勢無明顯變化,且以CD8+ T細胞浸潤為主的慢性炎癥反應持續存在,提示樹突細胞數量變化及成熟異常可能參與瞭COPD慢性炎癥遷延進展.
목적 관찰향연연무폭로대대서폐조직수돌세포수량、성숙도급폐조직만성염증변화적영향.방법 장30지웅성F344대서안수궤수자표법분위향연연무폭로조(폭로조)、단연조화건강대조조(대조조),매조10지.채용향연연무폭로법건립대서COPD모형,HE염색법검측대서기도염증병리평분급폐포평균내츤간격,면역조직화학ABC법관찰대서폐조직중CD11c+、CD86+화CD8+ T세포적분포급수량변화,류식세포술검측CD11c+/CD86+화CD11c+/주요조직상용성복합체(MHC)Ⅱ+여CD11c+수돌세포비치.결과 폭로조화단연조대서폐조직중출현COPD특정성병리개변,기도염증병리평분[(390±33)분화(324±28)분]급폐포평균내츤간격[(68±11)μm화(58±9)μm]명현고우대조조[(56±13)분화(36±6)μm],차이균유통계학의의(F치분별위459.85화34.03,균P＜0.05).폭로조화단연조대서CD11c+수돌세포양성솔[(1.47±0.12)%화(1.30±0.17)%]급CD86+수돌세포양성솔[(1.26±0.18)%화(1.02±0.08)%]균명현고우대조조[(0.96±0.08)%화(0.65±0.03)%],차이균유통계학의의(F치분별위6.55화30.26,균P＜0.05);폭로조화단연조대서CD8+T세포양성솔[(2.72±0.15)%화(2.35±0.23)%]균명현고우대조조[(1.39±0.11)%],차이유통계학의의(F=16.07,P＜0.05);폭로조화단연조대서CD11c+/CD86+수돌세포급CD11c+/MHCⅡ+수돌세포점CD11c+수돌세포비례[(5.5±0.4)%화(4.8±0.4)%]급[(4.2±0.3)%화(3.3±0.3)%]명현저우대조조[(8.0±0.5)%화(6.1±0.5)%],차이균유통계학의의(F치분별위14.34화12.82,균P＜0.05).폭로조여단연조상술각항지표비교,차이균무통계학의의(t치위1.10～2.11,균P＞0.05).결론 향연연무폭로유도COPD대서폐조직중수돌세포수량명현증가,성숙도명현하강,단연후차추세무명현변화,차이CD8+ T세포침윤위주적만성염증반응지속존재,제시수돌세포수량변화급성숙이상가능삼여료COPD만성염증천연진전.
Objective To evaluate the changes in the number and maturation of lung tissue dendritic cells (DCs) and to assess the chronic inflammation in a cigarette smoke-induced COPD model in rats.Methods Thirty male F344 rats were randomly divided into 3 groups (n = 10):a control group, a smoke-exposure group and a smoking cessation group.Rat lung pathomorphological changes were observed by hematoxylin-eosin (HE) stain.Lung tissue CD11c+ DCs, CD85+ DCs and CD8+ T cell numbers were observed by immunohistochemisty method.Flow cytometry was used for detection of CD11c+/CD86+ DCs and CD11c+/MHCⅡ + DCs proportions.Results The airway inflammatory pathological score and the mean linear intercept (MLI) obtained from he smoke-exposure group and the smoking cessation group (390 ± 33,324 + 28 ) and[(68 ± 11 ) μm, (58 ± 9) μm]were higher than those in the control group ( 56 ± 13 ) and ( 36 ± 6 ) μm( F =459.85 and 34.03, all P ＜0.05 ).In the smoke-exposure group and the smoking cessation group, the positive rate of CD11c+ DCs[(1.47 ±0.12)%, (1.30 ±0.17)%], and the positive rate of CD86+ DCs [( 1.26 ± 0.18 ) %, ( 1.02 ± 0.08 ) %]were higher than those in the control group[( 0.96 ± 0.08 ) %,(0.65 ± 0.03 ) %]( F = 6.55 and 30.26, all P ＜ 0.05 ), but there was no significant difference between the smoke-exposure group and the smoking cessation group ( t = 1.10 and 1.47, all P ＞ 0.05 ).In the smoke-exposure group and the smoking cessation group, CD8+ T positive rate[(2.72 ±0.15)%, (2.35 ±0.23)%]was higher than that in the control group[(1.39 ±0.11)%](F = 16.07, P ＜0.05).CD11c+/CD86+ DCs and CD11c+/MHC Ⅱ+DCs percentages[(5.5 ±0.4)%, (4.8 ±0.4)%],[(4.2 ±0.4)%, (3.3±0.3 )%]decreased in the smoke-exposure group and the smoking cessation group as compared to the control group[(8.0±0.5 ) %, (6.1 ± 0.5 ) %]( F = 14.34 and 12.82, all P ＜ 0.05 ).There was no significant difference between all the above index from the smoke-exposure group and the smoking cessation group ( t = 1.10 and 2.11, all P ＞ 0.05 ).Conclusions Cigarette smoke exposure induced increased DCs transmigrated and influenced the maturation of DCs in COPD rats.Even after smoking cessation, non-specific chronic inflammation was still present, suggesting that DCs number and maturation abnormality may be involved in the chronic inflammation of COPD.
