IL-13 induces translocation of NF-κB in cultured human bronchial smooth muscle cells

Background and purpose: Interleukin-13 (IL-13), a major Th2 cytokine, plays an important role in bronchial asthma, including mucus production, inflammation and airway hyperresponsiveness. Although IL-13 through its binding to IL-4 receptor α (IL-4Rα/IL-13Rα1 uses the canonical signal transducer and activator of transcription 6 (STAT6)-signaling pathway to mediate these tissue responses, recent studies have demonstrated that other signaling pathways may also be involved in. In the present study, whether IL-13 induces an activation of nuclear factor (NF)-κB, inflammatory transcription factor, was investigated in human bronchial smooth muscle cells (hBSMCs). Methods: Nuclear proteins were extracted from cultured hBSMCs treated with tumor necrosis factor (TNF)-α (10 ng/mL) or IL-13 (100 ng/mL), and assayed for activated NF-κB and STAT6 by Western blotting. Result: Treatments with TNF-α and IL-13 induced a translocation of NF-κB to nuclei in hBSMCs. In addition, coincubation with BMS-345541 (0.3 μM), an inhibitor of NF-κB (IκB) kinase (IKK) inhibitor, markedly inhibited the translocation of NF-κB. Conclusion: Our results suggest for the first time that IL-13 activates NF-κB in hBSMCs.