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‑α 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.