IL-13 induces translocation of NF-kappaB 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 alpha (IL-4Ralpha/IL-13Ralpha1 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)-kappaB, 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)-alpha (10 ng/mL) or IL-13 (100 ng/mL), and assayed for activated NF-kappaB and STAT6 by Western blotting.


RESULT
Treatments with TNF-alpha and IL-13 induced a translocation of NF-kappaB to nuclei in hBSMCs. In addition, coincubation with BMS-345541 (0.3 microM), an inhibitor of NF-kappaB (IkappaB) kinase (IKK) inhibitor, markedly inhibited the translocation of NF-kappaB.


CONCLUSION
Our results suggest for the first time that IL-13 activates NF-kappaB in hBSMCs.