Eosinophil trafficking and chronic tissue damage induced by allergic inflammation

C.计划的工作机构摘要 我们计划继续研究嗜酸性粒细胞相关疾病的血管生成和重塑。 创新领域：这些研究调查了在调节过敏原方面尚未探索的新途径 诱导的重塑(包括Del-1与血管内皮生长因子的相互作用；基质金属蛋白酶-7；内皮细胞和成纤维细胞的运输 祖细胞)，使用新的试剂(内皮细胞特异性敲除Del-1；Tie GFP和Col-1 GFP 用于跟踪内皮细胞和成纤维细胞祖细胞的转基因小鼠)和发现方法(蛋白质组学， 微阵列)以确定慢性和急性过敏原攻击肺中差异表达的基因/蛋白 (确定了几个候选人，包括WNT信号成员Kremin；miRNA376b)。除了可用性之外， 来自哮喘和EE的样本的研究允许这些发现被翻译到重塑的人类受试者身上。

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.