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Allergy and Airway: Asthma II |

Inhibitory Effects of PI3K Inhibitor on IL-25-Induced Allergen-Independent Asthma-Like Airways Remodelling

Ping Huang; Yan Li; Zhe Lv; Jingjing Wang; Yafei Chi; Qian Zhan; Xiujuan Yao; Chris Corrigan; Kewu Huang; Wei Wang; Sun Ying
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Capital Medical University, Beijing, China


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;149(4_S):A19. doi:10.1016/j.chest.2016.02.021
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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.

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