Feature Article: IL-25 contributes to lung fibrosis by directly acting on alveolar epithelial cells and fibroblasts.
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ABSTRACT: Impact statement
Our work focused on alveolar epithelial cells (AECs)-derived type-2 cytokine (interleukin [IL]-25) in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We showed that IL-25 and IL-17BR (IL-25's receptor) is upregulated in lung tissues (especially in AECs and lung fibroblasts) of IPF patients and contributes to lung fibrosis by directly activating lung fibroblasts and modulating epithelial-mesenchymal transition (EMT) of AECs. We suggest that IL-25 may be one of the master switches hidden in the milieu of abnormal epithelial-mesenchymal crosstalk. Treatment targeting IL-25 may be the potential and novel method for IPF patients.
SUBMITTER: Xu X
PROVIDER: S-EPMC6567590 | biostudies-literature | 2019 Jun
REPOSITORIES: biostudies-literature
Publications
IL-25 contributes to lung fibrosis by directly acting on alveolar epithelial cells and fibroblasts.
Xu Xuefeng X Luo Sa S Li Biyun B Dai Huaping H Zhang Jinglan J
Experimental biology and medicine (Maywood, N.J.) 20190418 9
<h4>Impact statement</h4>Our work focused on alveolar epithelial cells (AECs)-derived type-2 cytokine (interleukin [IL]-25) in the pathogenesis of idiopathic pulmonary fibrosis (IPF). We showed that IL-25 and IL-17BR (IL-25's receptor) is upregulated in lung tissues (especially in AECs and lung fibroblasts) of IPF patients and contributes to lung fibrosis by directly activating lung fibroblasts and modulating epithelial-mesenchymal transition (EMT) of AECs. We suggest that IL-25 may be one of th ...[more]
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