β-catenin regulates NF-κB activity and inflammatory cytokine expression in bronchial epithelial cells treated with lipopolysaccharide

Jang,Jaewoong; Ha,Jong-Hyeok; Chung,Sang-In; Yoon,Yoosik

doi:10.3892/ijmm.2014.1807

β-catenin regulates NF-κB activity and inflammatory cytokine expression in bronchial epithelial cells treated with lipopolysaccharide

Authors:
- Jaewoong Jang
- Jong-Hyeok Ha
- Sang-In Chung
- Yoosik Yoon
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Affiliations: Department of Microbiology, Chung-Ang University College of Medicine, Seoul 156-756, Republic of Korea
Published online on: June 16, 2014 https://doi.org/10.3892/ijmm.2014.1807
Pages: 632-638

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Abstract

In the present study, we demonstrate that lipopolysaccharide (LPS) induces the expression of inflammatory cytokines, including interleukin (IL)-6, IL-8, IL-1β, tumor necrosis factor (TNF)-α and monocyte chemoattractant protein (MCP)-1 in BEAS-2B human bronchial epithelial cells in a dose- and time-dependent manner. This increase was accompanied by an increased activity of nuclear factor (NF)‑κB. When the expression of β-catenin was analyzed following treatment with LPS, the mRNA level was unaltered; however, the β-catenin protein levels increased with a decrease in phosphorylation at the serine 33/37 residues. Nuclear β-catenin protein levels also increased along with the reporter activity of a β-catenin-responsive TOPFlash vector. To elucidate the regulatory role of β-catenin in the LPS-induced inflammatory response of bronchial epithelial cells, β-catenin production was knocked down using siRNA. Our results revealed that β-catenin protein levels and TOPFlash vector reporter activity were reduced to basal levels by siRNA transfection. In this experimental condition, NF-κB activity, measured by enzyme-linked immunosorbent assay (ELISA), electrophoretic mobility shift assay (EMSA) and an NF-κB responsive reporter assay, was reduced to basal levels. Similarly, LPS-induced inflammatory cytokine expression was reduced almost to basal levels following transfection with β-catenin siRNA. These results demonstrate that β-catenin positively regulates NF-κB activity, as well as the expression of inflammatory cytokines in the inflammatory response of LPS-treated bronchial epithelial cells.

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