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国家自然科学基金(KJ2009A80)

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相关作者:李静闻慧琴李小月罗庆礼王维更多>>
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Enhanced expression of the decoy receptor IL-13Rα2 in macrophages of Schistosomajaponicum-infected mice被引量:4
2009年
Background Type 2 cytokine interleukin (IL)-13 and its decoy receptor, IL-13 receptor (R)a2 appear to play a major role in tissue fibrosis of schistosomiasis and asthma. IL-13 is a key regulator of the extracellular matrix (ECM). It is known to signal to cells by binding to the IL-13Rα1, which then heterodimerizes with IL-4Rα. In contrast, IL-13Rα2 binds IL-13 with high affinity but does not signal. IL-13Rα2 is known to down-regulate granulomatous inflammation and prolong host survival in Schistosoma mansoni (S. mansoni) infection, but little is known about the location and expression level of IL-13Rα2 in the context of S. japonicum infection. Methods We established S. japonicum-infected mouse models. Kinetic serum levels of IL-13Rα2 were examined with ELISA. IL-13Rα2 mRNA and protein of liver tissues were determined by PCR and immunoblotting analysis, respectively. Detection of IL-13Rα2 expression and location in macrophages was performed by TaqMan PCR and fluorescent immunocytochemistry technique, respectively. Results A marked elevation of mRNA and protein expression of IL-13Rα2 was observed in mice during S. japonicum infection. An enhanced expression of IL-13Rα2 was further demonstrated in primary macrophages of murine schistosomiasis. Conclusions IL-13Rα2 in macrophages may be a critical contributor to pathogenesis of schistosomiasis. The data highlight the potential importance of cell signaling and antifibrotic gene therapeutics in T helper 2 cell (Th2)-mediated diseases.
WANG WeiSHEN Yu-xianLI JingZHANG Shi-haiLUO Qing-liZHONG Zhen-rongJIANG Zuo-junSHEN Ji-long
关键词:SCHISTOSOMIASISMACROPHAGES
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)被引量:1
2009年
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。
李静王维李小月储德勇闻慧琴周银娣张诗海罗庆礼沈继龙
关键词:IL-13NIH-3T3日本血吸虫病
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