Lipoteichoic acid upregulates NF-κB and proinflammatory cytokines by modulating β-catenin in bronchial epithelial cells.

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-1β, tumour necrosis factor-a and monocyte chemotactic protein-1, the upregulation of NF-κB, and the phosphorylation and degradation of I-κB. During the LTA-induced inflammatory response of the BEAS-2B human bronchial epithelial cells, the activity levels of the β-catenin-dependent promoter, and the protein expression levels of β-catenin were significantly upregulated, whereas β-catenin phosphorylation and the expression levels of AXIN were significantly downregulated. Following knockdown of β-catenin by small interfering (si)RNA transfection, both the LTA-induced protein expression levels of NF-κB and the LTA-induced activity levels of the NF-κB-dependent promoter were significantly reduced. Similarly, a marked reduction in I-κB phosphorylation and degradation was observed following β-catenin knockdown. The expression levels of the LTA-induced proinflammatory cytokines were also significantly reduced following β-catenin siRNA. These results suggest that β-catenin has a significant role in the regulation of NF-κB activity and proinflammatory cytokine expression during the LTA-induced inflammatory response of bronchial epithelial cells. [ABSTRACT FROM AUTHOR]