Diffuse Lung Disease: Diffuse Lung Disease: Interstitial Lung Disease |

The Expression and Role of IL-25 and Its Receptor in Idiopathic Pulmonary Fibrosis FREE TO VIEW

Xuefeng Xu, MD; Jing Geng, MD; Shuhong Li; Dingyuan Jiang, MD; Chen Wang, MD; Huaping Dai, MD
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Beijing Hospital, Beijing, China

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

Chest. 2016;149(4_S):A213. doi:10.1016/j.chest.2016.02.220
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SESSION TITLE: Diffuse Lung Disease: Interstitial Lung Disease

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a lethal disease with no proven drug treatment for blocking or reversing the decline of lung function. It is now believed that chronic injury of alveolar epithelial cells initiates IPF. Recent studies showed that IL-25, derived from the disregulated lung epithelial cells, can induce airway inflammation and remodeling which mimics human asthma. Thus, we aim to examine the expression of IL-25 and its receptor (IL-17RB/RA) in IPF lung tissues and their potential roles in regulating the pathogenesis of IPF.

METHODS: 4 normal and 6 IPF lung tissues were obtained. Immunohistochemistry (IHC), western blot, real time RT PCR assays were used to detect the expression of IL-25, IL-17RA/RB. Human embryonic lung fibroblast (MRC-5) was cultured and treated with exogenous IL-25. Cell proliferation was assessed by CCK-8/EDU assay. The expression of ECM proteins, profibrotic cytokines was detected by western blot, real time RT PCR.

RESULTS: We found that IL-25, IL-17RA/RB mRNA and protein level was remarkable higher in IPF lung tissues than that in normal controls. We also found that different dosage of IL-25 (1, 10, 100 ng/ml) significantly promoted the proliferation of MRC-5. Also, IL-25 augmented the expression of ECM proteins in MRC-5, including collagen I, collagen III, fibronectin as well as CTGF. Furthermore, IL-25 promoted MRC-5’s differentiation by upregulating α-SMA expression.

CONCLUSIONS: We concluded that IL-25 and IL-17RA/RB were upregulated in IPF lung tissues. IL-25 can activate human lung fibroblast by promoting its proliferation, differentiation, and ECM protein production. IL-25 may serve as a new potential target for IPF treatment.

CLINICAL IMPLICATIONS: This study may provide a novel clue and target for examine the pathogenesis and treatment of IPF.

DISCLOSURE: The following authors have nothing to disclose: Xuefeng Xu, Jing Geng, Shuhong Li, Dingyuan Jiang, Chen Wang, Huaping Dai

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