sIL-13Rα2抑制IL-13介导的NIH-3T3胶原I的合成及血吸虫病肝组织中sIL-13Rα2/IL-13的表达(英文)  

Inhibition of IL-13-induced collagen I by sIL-13Rα2 in NIH-3T3 fibroblast cells and the profile of sIL-13Rα2/IL-13 in mice with schistosomiasis

作　　者：李静[1,2] 王维[1,2] 李小月[1] 储德勇[2] 闻慧琴[1,2] 周银娣[1,2] 张诗海[1] 罗庆礼[1,2] 沈继龙[1,2] 

机构地区：[1]安徽省病原生物学省级实验室,教育部省部共建重要遗传病因资源利用重点实验室安徽医科大学,人兽共患病安徽省重点实验室(安徽医科大学),合肥230032 [2]安徽医科大学病原生物学教研室,合肥230032

出　　处：《中国人兽共患病学报》2009年第8期715-721,共7页Chinese Journal of Zoonoses

基　　金：Supported by the grant from the National Natural Science Foundation of China ( No .30571631 ;30872209);the grant from key provincial Natural Science Foundation of Anhui(KJ2009A80)

摘　　要：目的研究在成纤维细胞NIH-3T3中IL-13可溶性受体sIL-13Rα2对IL-13的抑制作用,为进一步研究sIL-13Rα2对日本血吸虫感染小鼠体内肝纤维化的治疗作用奠定基础。方法用ELISA和RT-PCR检测感染日本血吸虫的BALB/c小鼠0、6、8、10和12w不同感染时期肝脏组织IL-13和sIL-13Rα2表达和转录水平。构建sIL-13Rα2表达质粒转染成纤维细胞NIH-3T3,用IL-13(50ng/mL)刺激转染后成纤维细胞NIH-3T3,用RT-PCR和Western blotting分别检测该细胞分泌的Ⅰ型胶原。结果感染后小鼠肝脏肉芽肿组织中IL-13和sIL-13Rα2的蛋白表达水平随感染时间的延长而逐渐增高,第8wIL-13水平达到高峰(16.1586pg/mL),随后逐渐降低但仍高于正常水平(3.4146pg/mLP=0.017);第10wsIL-13Rα2的分泌达到高峰(4827.426pg/mL),以后逐渐减低,但仍高于正常水平(4057.112pg/mLP=0.021)。IL-13和sIL-13Rα2的mRNA转录趋势和ELISA检测结果相符合,均随感染时间的延长而增高,分别在第8w和第10w达到最高峰,随后逐渐降低但仍高于正常组小鼠(P=0.033;P=0.025)。实验组(sIL-13Rα2=2mg/mL)Ⅰ型胶原mRNA转录水平较正常对照组减低8.83%(P=0.012);蛋白水平较对照组减低7.41%(P=0.031)。结论sIL-13Rα2在NIH-3T3细胞中对IL-13有抑制作用,提示sIL-13Rα2在治疗血吸虫病肝纤维化中具有潜在价值。To determine the inhibition of IL-13 by recombinant sIL-13Rα2 in NIH-3T3 fibroblast cells for its potential therapeutic value in hepatic fibrosis caused by Schistosoma japanicum in mice . IL-13 and sIL-13Rα2 from liver of BALB/c mice infected with S. japonicum at different infection time （weeks 0,6,8,10 and 12） were analyzed by ELISA and RT-PCR. The recombinant sIL-13Rα2 expression plasmidwas constructed, followed by transfection into NIH-3T3 fibroblast cells. Type Ⅰ collagen produced by NIH-3T3 cells were examined by RT PCR and Western blotting. It was demonstrated that the expres sion of IL 13 increased gradually after infection, reached peak density （16. 1586 pg/mL）at week 8 and then reduced but was still higher than the level of control mice（3. 4146 pg/mL;P --0.017 ）. The secretion of sIL-13Rα2 reached to its peak 10 weeks after infection（4827. 426 pg/mL）and then reduced slowly but still higher than normal（4057. 112 pg/mL; P=0. 021）. Meanwhile, the changes in mRNA level of IL -13 and sIL-13Rα2 were coincided with that examined by ELISA. Both IL- 13 and sIL-13Rα2 reached their peak density （P=0. 033） at week 8 and 10 （P=0. 025） respectively, and they were followed by a slower degree of decrease. The sIL-13Rα2 could significantly inhibit the effect of IL-13 on NIH-3T3 fibroblast cells, showing decreased mRNA level（P = 0.012） and protein level of type Ⅰ collagen compared with normal groups（P =0.031 ）. It is concluded that the sIL-13Rα2 can inhibit the effect of IL 13 on NIH-3T3 fibroblast cells which leads to a reduced production of type Ⅰ collagen, demonstrating its potential therapeutic value in hepatic fibrosis of schistosomiasis.

关 键 词：sIL-13Rα2 IL-13 NIH-3T3 日本血吸虫病 肝纤维化 

分 类 号：R587.105[医药卫生—内分泌] R532.21[医药卫生—内科学]