中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2012年
16期
1129-1132
,共4页
黄颖%钟小宁%段敏超%唐海娟
黃穎%鐘小寧%段敏超%唐海娟
황영%종소저%단민초%당해연
肺气肿%白细胞介素21%小鼠%CD4阳性T淋巴细胞
肺氣腫%白細胞介素21%小鼠%CD4暘性T淋巴細胞
폐기종%백세포개소21%소서%CD4양성T림파세포
Pulmonary emphysema%Interleukin-21%Mice%CD4-positive T-lymphocytes
目的 探讨香烟烟雾暴露肺气肿小鼠肺部白细胞介素(IL)-21的变化及其对CD4+T细胞分化的影响.方法 20只雄性Balb/c小鼠随机分为对照组和烟熏组各10只.24周香烟烟雾暴露法建立小鼠肺气肿模型.HE染色观察小鼠肺组织的改变,计算平均内衬间隔和肺泡破坏指数;流式细胞术检测小鼠肺实质中CD4+IL-21R+T细胞比例;酶联免疫吸附测定(ELISA)检测小鼠肺实质中IL-21水平;分离烟熏组肺单个核细胞,分为空白组、共培养组2个亚组,后者与IL-21共培养,在24及48 h时分别通过流式细胞术检测Th1及Th17细胞比例.结果 烟熏组的平均内衬间隔和肺泡破坏指数[(48.6±4.8)μm和44.9±2.8]均显著高于对照组[(32.4±4.0)μm和28.1 ±2.1](均P<0.05).烟熏组肺实质中CD4+IL-21R+T细胞比例(4.1%±1.5%)较对照组(1.4%±0.4%)显著增高(P<0.05).烟熏组IL-21水平[(851±28) ng/L]较对照组[(415±39) ng/L]显著增高(P<0.05).小鼠肺实质中IL-21水平与平均内衬间隔、肺泡破坏指数呈显著正相关(r值分别为0.892和0.955,均P<0.05).在体外共培养24、48 h后共培养组Th17细胞及Th1细胞比例均显著高于空白组(均P<0.05).结论 IL-21可能通过诱导CD4+T细胞向Th1及Th17细胞分化,促进肺内Th1、Th17型细胞反应,参与肺气肿的形成与发展.
目的 探討香煙煙霧暴露肺氣腫小鼠肺部白細胞介素(IL)-21的變化及其對CD4+T細胞分化的影響.方法 20隻雄性Balb/c小鼠隨機分為對照組和煙熏組各10隻.24週香煙煙霧暴露法建立小鼠肺氣腫模型.HE染色觀察小鼠肺組織的改變,計算平均內襯間隔和肺泡破壞指數;流式細胞術檢測小鼠肺實質中CD4+IL-21R+T細胞比例;酶聯免疫吸附測定(ELISA)檢測小鼠肺實質中IL-21水平;分離煙熏組肺單箇覈細胞,分為空白組、共培養組2箇亞組,後者與IL-21共培養,在24及48 h時分彆通過流式細胞術檢測Th1及Th17細胞比例.結果 煙熏組的平均內襯間隔和肺泡破壞指數[(48.6±4.8)μm和44.9±2.8]均顯著高于對照組[(32.4±4.0)μm和28.1 ±2.1](均P<0.05).煙熏組肺實質中CD4+IL-21R+T細胞比例(4.1%±1.5%)較對照組(1.4%±0.4%)顯著增高(P<0.05).煙熏組IL-21水平[(851±28) ng/L]較對照組[(415±39) ng/L]顯著增高(P<0.05).小鼠肺實質中IL-21水平與平均內襯間隔、肺泡破壞指數呈顯著正相關(r值分彆為0.892和0.955,均P<0.05).在體外共培養24、48 h後共培養組Th17細胞及Th1細胞比例均顯著高于空白組(均P<0.05).結論 IL-21可能通過誘導CD4+T細胞嚮Th1及Th17細胞分化,促進肺內Th1、Th17型細胞反應,參與肺氣腫的形成與髮展.
목적 탐토향연연무폭로폐기종소서폐부백세포개소(IL)-21적변화급기대CD4+T세포분화적영향.방법 20지웅성Balb/c소서수궤분위대조조화연훈조각10지.24주향연연무폭로법건립소서폐기종모형.HE염색관찰소서폐조직적개변,계산평균내츤간격화폐포파배지수;류식세포술검측소서폐실질중CD4+IL-21R+T세포비례;매련면역흡부측정(ELISA)검측소서폐실질중IL-21수평;분리연훈조폐단개핵세포,분위공백조、공배양조2개아조,후자여IL-21공배양,재24급48 h시분별통과류식세포술검측Th1급Th17세포비례.결과 연훈조적평균내츤간격화폐포파배지수[(48.6±4.8)μm화44.9±2.8]균현저고우대조조[(32.4±4.0)μm화28.1 ±2.1](균P<0.05).연훈조폐실질중CD4+IL-21R+T세포비례(4.1%±1.5%)교대조조(1.4%±0.4%)현저증고(P<0.05).연훈조IL-21수평[(851±28) ng/L]교대조조[(415±39) ng/L]현저증고(P<0.05).소서폐실질중IL-21수평여평균내츤간격、폐포파배지수정현저정상관(r치분별위0.892화0.955,균P<0.05).재체외공배양24、48 h후공배양조Th17세포급Th1세포비례균현저고우공백조(균P<0.05).결론 IL-21가능통과유도CD4+T세포향Th1급Th17세포분화,촉진폐내Th1、Th17형세포반응,삼여폐기종적형성여발전.
Objective To evaluate the expression of interleukin (IL) -21 in a cigarette smoke-induced micemodel of emphysema and explorc its effects on the differentiation of CD4+T cell.Methods Twenty male Balb/c mice were randomly divided into two groups:control group and smoke-exposed group.Morphological changes were evaluated by mean linear intercepts and alveolar destructive index. The proportion of CD4+IL-21R+T cells in lungs of mice was determined by flow cytometry.And the levels of IL-21 in lungs of mice were analyzed by enzyme-linked immunosorbent assay (ELISA). Fresh lung mononuclear cells were isolated from the smoke-exposed group and divided further into two sub-groups:blank sub-group and co-culture sub-group.Two sub-groups were cultured in medium with or without IL-21 for 24 h and 48 h.The proportions of Th1 and Th17 cells in cell culture medium were determined by flow cytometry.Results Mean linear intercepts and alveolar destructive index in the smoke-exposed group ( (48.6 ± 4.8 )μm and 44.9 ± 2.8 ) were significantly higher than the control group ( ( 32.4 ± 4.0 ) μm and 28.1 ± 2.1,both P <0.05).In lungs,the percentage of CD4+IL-21R+T cells in the smoke-exposed group (4.1% ±1.5% ) significantly increased than that in the control group ( 1.4% ± 0.4% ) ( P < 0.05 ).The levels of IL-21 in lung of the smoke-exposed group ( (851 ± 28 ) ng/L) were higher than those in the control group ((415±39) ng/L,P <0.05).In lungs,the levels of IL-21 had positive correlations with mean linear intercepts and alvcolar destructive index ( r =0.892 and 0.955,both P < 0.05 ).The percentages of Th1and Th17 cells in cell culture medium of the co-culture suh-group for 24 h and 48 h significantly increased versus those in the blank group ( all P < 0.05 ).Conclusion IL-21 may participate in the occurrence and development of emphysema through the induced differentiation of CD4+T cells and the promotion of Th1 and Th17-cell responses in lungs.