SESSION TITLE: Asthma II
SESSION TYPE: Original Investigation Poster
PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM
PURPOSE: It is well known that IL-25 plays important role in the pathogenesis of asthma. We have previously shown that nasal challenge with IL-25 causes the airways accumulation of eosinophils, collagen deposition, mucus secretion and angiogenesis and other changes of airway remodelling in mice. In vitro, IL-25 induces expression of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) by human umbilical vein endothelial cells (HUVEC), which is possibly through PI3K signalling pathway because a pan PI3K inhibitor LY294002 abolishes IL-25-induced angiogenesis. In the present study, we hypothesized that PI3K inhibitor LY294002 is able to reduce IL-25-induced asthma-like airways inflammation, allergen-independent airway hyperresponsiveness (AHR) and airways remodelling in vivo.