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 extracellul...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.展开更多
基金This work was supported by Natural Science Foundation of Anhui Educational Committee （No. KJ2009A80）.
文摘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.
