Activation of Eosinophil CCR3 Signaling and Eotaxin Using a Bioinformatics Analysis of a Mouse Model of Obliterative Airway Disease

摘要: The role of eosinophils in the development and progression chronic allograft rejection is recognized multiple organ transplantation settings. CCR3 signaling pathway one key regulatory pathways eosinophil migration to engrafted tissue. Eotaxin a ligand for reflects eosinophilic inflammation, which can lead fibrosis. We hypothesized that would be upregulated obliterative airway disease (OAD) an established model rejection. mouse gene microarray data from heterotopic OAD NIH Gene Expression Omnibus (GEO) repository were analyzed differentially expressed pathways, using Partek Suite Ingenuity Pathway Analysis. A P value <0.005 was defined as significant differential expression, <0.05 pathways. Day 25 allografts day 4 acute isografts at showed upregulation (P=0.04), based on analysis 1,299 uniquely genes. compared with those identification 1,859 unique genes, there trend toward over time (P=0.06). not during alloimmune versus comparison, 1,603 by 2.5-fold. eotaxin significantly our results imply controlling early damage controls.