中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
42期
6763-6768
,共6页
组织构建%组织工程%实验性自身免疫性脑脊髓炎%视神经炎%辅助性T细胞亚群%白细胞介素4%白细胞介素17%干扰素γ%Foxp3%炎症损伤%发病机制%病理改变
組織構建%組織工程%實驗性自身免疫性腦脊髓炎%視神經炎%輔助性T細胞亞群%白細胞介素4%白細胞介素17%榦擾素γ%Foxp3%炎癥損傷%髮病機製%病理改變
조직구건%조직공정%실험성자신면역성뇌척수염%시신경염%보조성T세포아군%백세포개소4%백세포개소17%간우소γ%Foxp3%염증손상%발병궤제%병리개변
tissue engineering%T-lymphocytes%autoimmunity%T-lymphocyte subsets
背景:视神经炎的病因多为自身免疫引起的炎性脱髓鞘,很多的视神经炎为多发性硬化的早期表现。在外周CD4+T细胞中,有5%-10%为调节性T细胞,其免疫抑制能力很强。自身免疫性脑脊髓炎所引起的视神经炎发病机制是否与辅助性T细胞亚群的有关呢?目的:分析实验性自身免疫性脑脊髓炎小鼠模型视神经炎发病机制与辅助性T细胞亚群的关系。方法:将小鼠腹腔注射百日咳菌液建立实验性自身免疫性脑脊髓炎模型,分别免疫11,15,19 d,并设腹腔注射生理盐水的佐剂组小鼠作对照。<br> 结果与结论:酶联免疫吸附检测显示,与佐剂组相比,免疫后19 d组视神经白细胞介素4蛋白含量降低(P<0.05);免疫后11,15 d组视神经白细胞介素17蛋白含量升高(P<0.05);免疫后15,19 d组视神经干扰素γ蛋白含量升高(P <0.05);免疫后11,15,19 d组视神经Foxp3蛋白含量显著降低(P <0.05)。实时PCR检测显示,与佐剂组相比,免疫后11,15,19 d组视神经中干扰素γ、Foxp3 mRNA表达降低(P<0.05), RORt mRNA表达升高;免疫后15,19 d组视神经中白细胞介素4,白细胞介素17,T-beat mRNA表达升高(P<0.05)。免疫后19 d组GATA3 mRNA表达降低(P<0.05)。结果证实,实验性自身免疫性脑脊髓炎小鼠模型视神经炎的发生发展可能受到Foxp3和调节性T细胞表达减少的影响,免疫后早期白细胞介素17可能介导对炎症损伤,发病高峰期干扰素γ可能使炎症损伤程度加重。
揹景:視神經炎的病因多為自身免疫引起的炎性脫髓鞘,很多的視神經炎為多髮性硬化的早期錶現。在外週CD4+T細胞中,有5%-10%為調節性T細胞,其免疫抑製能力很彊。自身免疫性腦脊髓炎所引起的視神經炎髮病機製是否與輔助性T細胞亞群的有關呢?目的:分析實驗性自身免疫性腦脊髓炎小鼠模型視神經炎髮病機製與輔助性T細胞亞群的關繫。方法:將小鼠腹腔註射百日咳菌液建立實驗性自身免疫性腦脊髓炎模型,分彆免疫11,15,19 d,併設腹腔註射生理鹽水的佐劑組小鼠作對照。<br> 結果與結論:酶聯免疫吸附檢測顯示,與佐劑組相比,免疫後19 d組視神經白細胞介素4蛋白含量降低(P<0.05);免疫後11,15 d組視神經白細胞介素17蛋白含量升高(P<0.05);免疫後15,19 d組視神經榦擾素γ蛋白含量升高(P <0.05);免疫後11,15,19 d組視神經Foxp3蛋白含量顯著降低(P <0.05)。實時PCR檢測顯示,與佐劑組相比,免疫後11,15,19 d組視神經中榦擾素γ、Foxp3 mRNA錶達降低(P<0.05), RORt mRNA錶達升高;免疫後15,19 d組視神經中白細胞介素4,白細胞介素17,T-beat mRNA錶達升高(P<0.05)。免疫後19 d組GATA3 mRNA錶達降低(P<0.05)。結果證實,實驗性自身免疫性腦脊髓炎小鼠模型視神經炎的髮生髮展可能受到Foxp3和調節性T細胞錶達減少的影響,免疫後早期白細胞介素17可能介導對炎癥損傷,髮病高峰期榦擾素γ可能使炎癥損傷程度加重。
배경:시신경염적병인다위자신면역인기적염성탈수초,흔다적시신경염위다발성경화적조기표현。재외주CD4+T세포중,유5%-10%위조절성T세포,기면역억제능력흔강。자신면역성뇌척수염소인기적시신경염발병궤제시부여보조성T세포아군적유관니?목적:분석실험성자신면역성뇌척수염소서모형시신경염발병궤제여보조성T세포아군적관계。방법:장소서복강주사백일해균액건립실험성자신면역성뇌척수염모형,분별면역11,15,19 d,병설복강주사생리염수적좌제조소서작대조。<br> 결과여결론:매련면역흡부검측현시,여좌제조상비,면역후19 d조시신경백세포개소4단백함량강저(P<0.05);면역후11,15 d조시신경백세포개소17단백함량승고(P<0.05);면역후15,19 d조시신경간우소γ단백함량승고(P <0.05);면역후11,15,19 d조시신경Foxp3단백함량현저강저(P <0.05)。실시PCR검측현시,여좌제조상비,면역후11,15,19 d조시신경중간우소γ、Foxp3 mRNA표체강저(P<0.05), RORt mRNA표체승고;면역후15,19 d조시신경중백세포개소4,백세포개소17,T-beat mRNA표체승고(P<0.05)。면역후19 d조GATA3 mRNA표체강저(P<0.05)。결과증실,실험성자신면역성뇌척수염소서모형시신경염적발생발전가능수도Foxp3화조절성T세포표체감소적영향,면역후조기백세포개소17가능개도대염증손상,발병고봉기간우소γ가능사염증손상정도가중。
BACKGROUND:More and more evidence have shown that autoimmune-induced inflammatory demyelinating mostly leads to optic neuritis that is quite an early manifestation of multiple sclerosis, but whether the pathogenesis of optic neuritis in experimental autoimmune encephalomyelitis (EAE) mice is correlated with helper T cellsubsets has rarely been reported. <br> OBJECTIVE:To analyze the correlation between pathogenesis of optic neuritis of mouse EAE model with helper T cellsubsets. <br> METHODS:The mice were injected intraperitoneal y Bordetel a pertussis to establish EAE models. Then, the animal models were subjected to immunization for 11, 15, 19 days, respectively. Mice undergoing intraperitoneal injection of normal saline served as controls (adjuvant group). <br> RESULTS AND CONCLUSION:Compared with the adjuvant group, the protein expression of interleukin 4 in the optic nerve decreased in the 19-day immunization group (P<0.05);the protein expression of interleukin 17 in the optic nerve increased in the 11-and 15-day immunization groups (P<0.05);the protein expression of interferonγin the optic nerve increased in the 15-and 19-day immunization groups (P<0.05);the protein expression of Foxp3 in the optic nerve decreased in the 11-, 15-and 19-day immunization groups (P<0.05). Real-time PCR results showed that compared with the adjuvant group, the mRNA expression of interferonγand Foxp3 in the optic nerve decreased (P<0.05), while mRNA expression of RORt increased in the 11-, 15-and 19-day immunization groups;the mRNA expression of interleukin 4, interleukin 17, T-beat increased in the 15-and 19-day immunization groups (P<0.05);the mRNA expression of GATA3 reduced in the 19-day immunization group (P<0.05). These results reveal that Foxp3 expression and helper T cellreduction have important influences on the development of optic neuritis in EAE mouse models, interleukin 17 may mediates inflammatory injury in the early stage, while interferon-γmakes inflammatory injury worse in the peak incidence of the disease.