Eosinophil trafficking and chronic tissue damage induced by allergic inflammation

C.计划工作内容摘要 我们计划继续研究嗜酸性粒细胞相关疾病中的血管生成和重塑。 创新领域：这些研究调查了在介导过敏原方面尚未探索的新途径 诱导的重塑（包括与VEGF相互作用的Del-1; MMP-7;内皮细胞和成纤维细胞的运输 祖细胞），使用新试剂（Del-1的内皮细胞特异性敲除; Tie GFP和Col-1 GFP 转基因小鼠以追踪内皮和成纤维细胞祖细胞），和发现方法（蛋白质组学， 微阵列）以鉴定慢性与急性变应原攻击的肺中差异表达的基因/蛋白质 （鉴定了几种候选物，包括Wnt信号传导成员Kremin; miRNA 376 b）。此外，可用性 从哮喘和EE标本的研究结果可以被翻译到人类受试者与重塑。

C. ABSTRACT OF PLANNED BODY OF WORK We plan to continue our studies of angiogenesis and remodeling in eosinophil associated diseases. Areas of innovation: The studies investigate novel pathways that are unexplored in mediating allergen induced remodeling (including Del-1 interacting with VEGF; MMP-7; trafficking of endothelial and fibroblast progenitors), use novel reagents (endothelial cell specific knockout of Del-1; Tie GFP and Col-1 GFP transgenic mice to track endothelial and fibroblast progenitors), and discovery approaches (proteomics, microarray) to identify differentially expressed genes/proteins in chronic vs acute allergen challenged lung (identified several candidates including Wnt signaling member Kremin; miRNA376b). In addition the availability of specimens from asthma and EE allow the findings to be translated to human subjects with remodeling.