中华肝胆外科杂志
中華肝膽外科雜誌
중화간담외과잡지
CHINESE JOURNAL OF HEPATOBILIARY SURGERY
2010年
8期
616-619
,共4页
侯静%唐大年%许媛%韦军民
侯靜%唐大年%許媛%韋軍民
후정%당대년%허원%위군민
次黄嘌呤单核苷酸脱氢酶抑制剂%趋化因子%迁移%吞噬
次黃嘌呤單覈苷痠脫氫酶抑製劑%趨化因子%遷移%吞噬
차황표령단핵감산탈경매억제제%추화인자%천이%탄서
Inosine monophosphate dehydrogenase inhibitor%Chemokine%Migration%Endocytosis
目的 探讨次黄嘌呤单核苷酸脱氢酶抑制剂(Inosine monophosphate dehydrogenase inhibitor,IMPDHI)对人外周髓样树突状细胞(Myeloid dendritic cells,MDC)趋化、迁移、吞噬功能的影响.方法 新鲜外周血单个核细胞来源于健康志愿者(N=15).实验组加入不同浓度IMPDHI,流式细胞仪分析MDC表面趋化因子受体表达水平.于transwell小室实验中,加入不同的化学因子,经Lin-1/CD11c/HLA-DR染色后,流式细胞仪计数,以迁移细胞的百分比表示迁移能力.分离树突状细胞抗原-1+(Blood dendritic cell antigen-1,BDCA-1+)细胞后,以甘露糖受体作为介导,流式细胞仪测定BDCA-1+细胞中FITC标记的右旋糖酐的荧光值表示吞噬能力.结果 (1)趋化、迁移功能:与对照组相比,实验组MDC的趋化因子受体CCR1表达水平明显升高(17.02±3.23～30.63±9.13,P＜0.05);CCR3表达水平(10.26±2.25～5.81±0.97,P＜0.05)和CCR7表达水平(9.56±1.84～5.18±0.60,P＜0.05)明显下降.实验组MDC对炎性化学因子CCL2、CCL3、CCL4、CCL7、CXCL12的趋化能力明显增强(P＜0.05),对淋巴器官性化学因子CCL19、CCL20、CCL21、CXCL11的趋化能力无明显改变(P＞0.05).(2)吞噬功能:实验组MDC的吞噬能力明显强于对照组(P＜0.05).结论 IMPDHI增强MDC吞噬抗原的能力,通过提高MDC炎性化学因子受体的表达水平和增强其对炎性化学因子的趋化能力,抑制MDC对淋巴器官的趋化、迁移能力.
目的 探討次黃嘌呤單覈苷痠脫氫酶抑製劑(Inosine monophosphate dehydrogenase inhibitor,IMPDHI)對人外週髓樣樹突狀細胞(Myeloid dendritic cells,MDC)趨化、遷移、吞噬功能的影響.方法 新鮮外週血單箇覈細胞來源于健康誌願者(N=15).實驗組加入不同濃度IMPDHI,流式細胞儀分析MDC錶麵趨化因子受體錶達水平.于transwell小室實驗中,加入不同的化學因子,經Lin-1/CD11c/HLA-DR染色後,流式細胞儀計數,以遷移細胞的百分比錶示遷移能力.分離樹突狀細胞抗原-1+(Blood dendritic cell antigen-1,BDCA-1+)細胞後,以甘露糖受體作為介導,流式細胞儀測定BDCA-1+細胞中FITC標記的右鏇糖酐的熒光值錶示吞噬能力.結果 (1)趨化、遷移功能:與對照組相比,實驗組MDC的趨化因子受體CCR1錶達水平明顯升高(17.02±3.23～30.63±9.13,P＜0.05);CCR3錶達水平(10.26±2.25～5.81±0.97,P＜0.05)和CCR7錶達水平(9.56±1.84～5.18±0.60,P＜0.05)明顯下降.實驗組MDC對炎性化學因子CCL2、CCL3、CCL4、CCL7、CXCL12的趨化能力明顯增彊(P＜0.05),對淋巴器官性化學因子CCL19、CCL20、CCL21、CXCL11的趨化能力無明顯改變(P＞0.05).(2)吞噬功能:實驗組MDC的吞噬能力明顯彊于對照組(P＜0.05).結論 IMPDHI增彊MDC吞噬抗原的能力,通過提高MDC炎性化學因子受體的錶達水平和增彊其對炎性化學因子的趨化能力,抑製MDC對淋巴器官的趨化、遷移能力.
목적 탐토차황표령단핵감산탈경매억제제(Inosine monophosphate dehydrogenase inhibitor,IMPDHI)대인외주수양수돌상세포(Myeloid dendritic cells,MDC)추화、천이、탄서공능적영향.방법 신선외주혈단개핵세포래원우건강지원자(N=15).실험조가입불동농도IMPDHI,류식세포의분석MDC표면추화인자수체표체수평.우transwell소실실험중,가입불동적화학인자,경Lin-1/CD11c/HLA-DR염색후,류식세포의계수,이천이세포적백분비표시천이능력.분리수돌상세포항원-1+(Blood dendritic cell antigen-1,BDCA-1+)세포후,이감로당수체작위개도,류식세포의측정BDCA-1+세포중FITC표기적우선당항적형광치표시탄서능력.결과 (1)추화、천이공능:여대조조상비,실험조MDC적추화인자수체CCR1표체수평명현승고(17.02±3.23～30.63±9.13,P＜0.05);CCR3표체수평(10.26±2.25～5.81±0.97,P＜0.05)화CCR7표체수평(9.56±1.84～5.18±0.60,P＜0.05)명현하강.실험조MDC대염성화학인자CCL2、CCL3、CCL4、CCL7、CXCL12적추화능력명현증강(P＜0.05),대림파기관성화학인자CCL19、CCL20、CCL21、CXCL11적추화능력무명현개변(P＞0.05).(2)탄서공능:실험조MDC적탄서능력명현강우대조조(P＜0.05).결론 IMPDHI증강MDC탄서항원적능력,통과제고MDC염성화학인자수체적표체수평화증강기대염성화학인자적추화능력,억제MDC대림파기관적추화、천이능력.
Objective To study the effect of inosine monophosphate dehydrogenase inhibitor (IMPDHI) on chemotaxis, migration and endocytosis of human peripheral myeloid dendritic cells (MDCs). Methods Freshly isolated peripheral blood mononuclear cells(PBMC)collected from healthy volunteers (N=15) and the study group were treated with IMPDHI. CC chemokine receptors on MDCs were analyzed by flow cytometry. The study group, control group and different chemokines were added via trans-well approach for different chemokines, stained by Lin-1/CD11c/HLA-DR and counted by flow cytometry. The migration index was calculated as a percentage of MDC migrated in response to the tested chemokine. After isolation of blood dendritic cell antigen-1+ (BDCA-1+ ), mannose receptor-mediated endocytosis was measured as the cellular uptake of FITC-dextran by the flow cytometry. Results (1) Compared to the control group, the expression of CCR1 in the study group was up-regulated significantly(17.02±3.23～30.63±9.13, P＜0.05) and the expressions of CCR3(10.26±2.25～5.81±0.97 P＜0.05) and CCR7 (9.56± 1.84～5.18±0.60 P＜0.05)were downregulated significantly. MDCs in the study group showed enhanced migratory response to inflammatory chemokine CCL2, CCL3, CCL4, CCL7 and CXCL12 (P＜0.05). (2)The endocytosis capacity in the study group was significantly higher than that in control group (P ＜0.05). Conclusion IMPDHI enhances the endocytotic capacity of MDCs and impairs the migratory response of peripheral MDCs to lymphocytic tissue by up-regulating the expression of chemokine receptor in MDCs and enhancing migratory response to inflammatory chemokines.
