中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
2期
284-287
,共4页
CD4+ CD25+调节性T细胞%辅助性T细胞17%脓毒症
CD4+ CD25+調節性T細胞%輔助性T細胞17%膿毒癥
CD4+ CD25+조절성T세포%보조성T세포17%농독증
CD4+ CD25+ regulatory T cells%T helper type 17 cells%Sepsis
目的 观察CD4+ CD25+调节T细胞(Treg)/辅助性T细胞17(Th17)细胞在脓毒症大鼠炎性免疫反应中的作用.方法 110只雄性SD大鼠随机分为正常对照组、假手术组、脓毒症(CLP)组,采用改良的盲肠结扎穿孔术(CLP)制作大鼠脓毒症模型.采用流式细胞术检测CD14+单核细胞表面人类白细胞抗原-DR基因(HLA-DR)表达率、Treg细胞及TH17细胞比例;酶联免疫吸附试验(ELISA)检测白细胞介素(IL)-6、IL-10、肿瘤坏死因子(TNF)-α、转化生长因子(TGF)-β、白细胞介素(IL)-17炎性因子蛋白表达.结果 与假手术组比较:(1)伴随着脓毒症病情的发展,大鼠出现明显的免疫抑制,CD14+单核细胞HLA-DR表达率＜30％,IL-10/TNF-α比值(27.41 ±7.04比6.63 ±2.60)明显增高(P＜0.01).(2)术后96 h脓毒症大鼠Treg细胞[(11.91±3.88)％比(6.57±2.60)％,P＜0.01]和Th17细胞[(5.14±0.29)％比(2.85±0.07)％,P＜0.01]表达明显增高.(3)术后96 h脓毒症组前炎性细胞因子IL-6[(42.31±15.89) ng/L比(6.32 ±3.18) ng/L,P＜0.01]、IL-10[(69.89 ±20.78) ng/L比(13.58±5.37) ng/L,P＜0.01]、TNF-α[(5.03±3.10) ng/L比(2.77±1.10) ng/L,P＜0.01]、TGF-β[(4.99±2.01) ng/L比(1.88±1.07) ng/L,P＜0.01]、IL-17[(92.77±11.64) ng/L比(7.58±2.30) ng/L,P＜0.01]表达明显增高.结论 伴随着脓毒症病情的发展,大鼠出现明显的免疫抑制;在大鼠脓毒症的发生发展中,Treg细胞介导的免疫抑制及Th17细胞介导免疫激活反应同时存在;脓毒症细胞因子微环境变化可能是导致Treg细胞/Th17细胞失衡的原因之一.
目的 觀察CD4+ CD25+調節T細胞(Treg)/輔助性T細胞17(Th17)細胞在膿毒癥大鼠炎性免疫反應中的作用.方法 110隻雄性SD大鼠隨機分為正常對照組、假手術組、膿毒癥(CLP)組,採用改良的盲腸結扎穿孔術(CLP)製作大鼠膿毒癥模型.採用流式細胞術檢測CD14+單覈細胞錶麵人類白細胞抗原-DR基因(HLA-DR)錶達率、Treg細胞及TH17細胞比例;酶聯免疫吸附試驗(ELISA)檢測白細胞介素(IL)-6、IL-10、腫瘤壞死因子(TNF)-α、轉化生長因子(TGF)-β、白細胞介素(IL)-17炎性因子蛋白錶達.結果 與假手術組比較:(1)伴隨著膿毒癥病情的髮展,大鼠齣現明顯的免疫抑製,CD14+單覈細胞HLA-DR錶達率＜30％,IL-10/TNF-α比值(27.41 ±7.04比6.63 ±2.60)明顯增高(P＜0.01).(2)術後96 h膿毒癥大鼠Treg細胞[(11.91±3.88)％比(6.57±2.60)％,P＜0.01]和Th17細胞[(5.14±0.29)％比(2.85±0.07)％,P＜0.01]錶達明顯增高.(3)術後96 h膿毒癥組前炎性細胞因子IL-6[(42.31±15.89) ng/L比(6.32 ±3.18) ng/L,P＜0.01]、IL-10[(69.89 ±20.78) ng/L比(13.58±5.37) ng/L,P＜0.01]、TNF-α[(5.03±3.10) ng/L比(2.77±1.10) ng/L,P＜0.01]、TGF-β[(4.99±2.01) ng/L比(1.88±1.07) ng/L,P＜0.01]、IL-17[(92.77±11.64) ng/L比(7.58±2.30) ng/L,P＜0.01]錶達明顯增高.結論 伴隨著膿毒癥病情的髮展,大鼠齣現明顯的免疫抑製;在大鼠膿毒癥的髮生髮展中,Treg細胞介導的免疫抑製及Th17細胞介導免疫激活反應同時存在;膿毒癥細胞因子微環境變化可能是導緻Treg細胞/Th17細胞失衡的原因之一.
목적 관찰CD4+ CD25+조절T세포(Treg)/보조성T세포17(Th17)세포재농독증대서염성면역반응중적작용.방법 110지웅성SD대서수궤분위정상대조조、가수술조、농독증(CLP)조,채용개량적맹장결찰천공술(CLP)제작대서농독증모형.채용류식세포술검측CD14+단핵세포표면인류백세포항원-DR기인(HLA-DR)표체솔、Treg세포급TH17세포비례;매련면역흡부시험(ELISA)검측백세포개소(IL)-6、IL-10、종류배사인자(TNF)-α、전화생장인자(TGF)-β、백세포개소(IL)-17염성인자단백표체.결과 여가수술조비교:(1)반수착농독증병정적발전,대서출현명현적면역억제,CD14+단핵세포HLA-DR표체솔＜30％,IL-10/TNF-α비치(27.41 ±7.04비6.63 ±2.60)명현증고(P＜0.01).(2)술후96 h농독증대서Treg세포[(11.91±3.88)％비(6.57±2.60)％,P＜0.01]화Th17세포[(5.14±0.29)％비(2.85±0.07)％,P＜0.01]표체명현증고.(3)술후96 h농독증조전염성세포인자IL-6[(42.31±15.89) ng/L비(6.32 ±3.18) ng/L,P＜0.01]、IL-10[(69.89 ±20.78) ng/L비(13.58±5.37) ng/L,P＜0.01]、TNF-α[(5.03±3.10) ng/L비(2.77±1.10) ng/L,P＜0.01]、TGF-β[(4.99±2.01) ng/L비(1.88±1.07) ng/L,P＜0.01]、IL-17[(92.77±11.64) ng/L비(7.58±2.30) ng/L,P＜0.01]표체명현증고.결론 반수착농독증병정적발전,대서출현명현적면역억제;재대서농독증적발생발전중,Treg세포개도적면역억제급Th17세포개도면역격활반응동시존재;농독증세포인자미배경변화가능시도치Treg세포/Th17세포실형적원인지일.
Objective To investigate the roles of CD4+ CD25 + regulatory T cells (Treg) and T helper type 17 (Th17) cells in inflammatory response in septic rats.Methods A total of 110 healthy male Sprague-Dawley rats (250-300 g) were randomly divided into 3 groups:normal control group,sham group and cecal ligation and puncture (CLP) group.The rat models of sepsis were established by improved CLP.Flow cytometric analysis was performed to detect the percentage of CD14 + T cell,Th17 cells and Treg cells subpopulation.Expressions of proinflammatory cytokines [interleukin (IL)-6,IL-10,tumor necrosis factor (TNF)-α,transforming growth factor (TGF)-β,IL-17] were measured by using enzyme-linked immunosorbent serologic assay.Results Compared with sham group,(1) While the spesis becoming worse,the rats were immunological inhibition,the expression levels of leucocyte antigen-DR (19.63 ± 7.56) ％ lower than 30％ and the rate of IL-10/TNF-α (27.41 ± 7.04 vs.6.63 ± 2.60,P ＜0.01) significantly up-regulated.(2) After 96 hours,the proportions of Treg cells [(11.91 ± 3.88)％ vs.(6.57±2.60)％,P＜0.01] andTh17 cells [(5.14 ±0.29)％ vs.(2.85 ±0.07)％,P ＜0.01] in sepsis group were significantly higher.(3) After 96 hours,the expression levels of IL-6 [(42.31 ±15.89) ng/Lvs.(6.32 ±3.18) ng/L,P＜0.01],IL-10 [(69.89 ±20.78) ng/L vs.(13.58±5.37) ng/L,P＜0.01],TNF-α [(5.03 ±3.10) ng/L vs.(2.77 ±1.10) ng/L,P＜ 0.01],TGF-β [(4.99±2.01) ng/L vs.(1.88±1.07) ng/L,P＜0.01],IL-17 [(92.77±11.64) ng/L vs.(7.58 ±2.30) ng/L,P ＜0.01] were significantly up-regulated in sepsis group.Conclusion While the spesis becoming worse,the rats were immunological inhibition.Aberrant activation of Th17 cells and Treg cells might be involved in pathogenesis in sepsis.The changes of cytokine environment in sepsis may be one of the factors causing the imbalance of Treg cells/Th17 cells.
