Enhanced expression of the decoy receptor IL-13Rα2 in macrophages of Schistosomajaponicum-infected mice  被引量:4

Enhanced expression of the decoy receptor IL-13Rα2 in macrophages of Schistosomajaponicum-infected mice

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作  者:WANG Wei SHEN Yu-xian LI Jing ZHANG Shi-hai LUO Qing-li ZHONG Zhen-rong JIANG Zuo-jun SHEN Ji-long 

机构地区:[1]Department of Epidemiology and Biostatistics, School of Public Health [2]Department of Pathobiology, Anhui Medical University, Hefei, Anhui 230032, China [3]Key Laboratory of Gene Resource Utilization for Severe Diseases, the Ministry of Education of China and Anhui Province, Hefei 230032, China

出  处:《Chinese Medical Journal》2009年第14期1650-1654,共5页中华医学杂志(英文版)

基  金:This work was supported by Natural Science Foundation of Anhui Educational Committee (No. KJ2009A80).

摘  要: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.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.

关 键 词:SCHISTOSOMIASIS MACROPHAGES interleukin-13R 

分 类 号:R686[医药卫生—骨科学]

 

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