Lipoteichoic acid upregulates NF-kappa B and proinflammatory cytokines by modulating beta-catenin in bronchial epithelial cells

Abstract

Lipoteichoic acid (LTA) is a major cell wall component and virulence factor of gram-positive bacteria. The present study investigated the LTA-induced inflammatory response of BEAS-2B human bronchial epithelial cells, and detected the expression levels of proinflammatory cytokines interleukin (IL)-6, IL-8, IL-1 beta, tumour necrosis factor-a and monocyte chemotactic protein-1, the upregulation of NF-kappa B, and the phosphorylation and degradation of I-kappa B. During the LTA-induced inflammatory response of the BEAS-2B human bronchial epithelial cells, the activity levels of the beta-catenin-dependent promoter, and the protein expression levels of beta-catenin were significantly upregulated, whereas beta-catenin phosphorylation and the expression levels of AXIN were significantly downregulated. Following knockdown of beta-catenin by small interfering (si) RNA transfection, both the LTA-induced protein expression levels of NF-kappa B and the LTA-induced activity levels of the NF-kappa B-dependent promoter were significantly reduced. Similarly, a marked reduction in I-kappa B phosphorylation and degradation was observed following beta-catenin knockdown. The expression levels of the LTA-induced proinflammatory cytokines were also significantly reduced following beta-catenin siRNA. These results suggest that beta-catenin has a significant role in the regulation of NF-kappa B activity and proinflammatory cytokine expression during the LTA-induced inflammatory response of bronchial epithelial cells.