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Interleukin‐13 promotes expression of Alix to compromise renal tubular epithelial barrier function
Author(s) -
Xu Chen,
Sun Guangdong,
Yang Jie,
Sun Qianmei,
Tong Zhaohui
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10433
Subject(s) - barrier function , microbiology and biotechnology , chemistry , epithelium , biology , genetics
The epithelial barrier dysfunction plays a critical role in a number of kidney diseases. The mechanism is unclear. Alix is a protein involving in protein degradation in epithelial cells. This study aims to investigate that interleukin (IL)‐13 inhibits Alix to compromise the kidney epithelial barrier function. In this study, the murine collecting duct cell line (M‐1) was cultured in Transwell inserts to investigate the significance of Alix in compromising the epithelial barrier functions. T cell (Teff cells) proliferation assay was employed to assess the antigenicity of ovalbumin (OVA) that was transported across the M‐1 monolayer barrier. The results showed that M‐1 cells express Alix. Exposure to interleukin (IL)‐13 markedly decreased the expression of Alix in M‐1 cells, which compromised the M‐1 monolayer barrier functions by showing the increases in the permeability to OVA. Over‐expression of Alix abolished the IL‐13‐induced M‐1 monolayer barrier dysfunction. Knockdown of Alix significantly increased M‐1 monolayer permeability. The OVA collected from the Transwell basal chambers induced the OVA‐specific T cell proliferation. We conclude that IL‐13 compromises M‐1 epithelial barrier functions via inhibiting Alix expression.