J Rhinol.  2007 Nov;14(2):100-105.

IL-1beta Induces Lysozyme Overexpression through a Mechanism Involving ERK/p38 Mitogen Activated Protein Kinase Activation in Human Airway Epithelial Cells

  • 1Department of Otorhinolaryngology, Yonsei University, College of Medicine, Seoul, Korea.
  • 2The Airway Mucus Institute, Yonsei University, College of Medicine, Seoul, Korea.


BACKGROUND AND OBJECTIVES: Lysozyme, a major serous component of airway epithelial secretions, plays an important role in airway defense. However, little is understood about the regulation of its expression and the associated signaling pathway. The object of this study is to investigate the regulation of lysozyme expression, the downstream signaling pathway of lysozyme expression, and the related protein kinases under inflammatory conditions using the IL-1beta, which acts as a significant cytokine in many airway inflammations.
After the IL-1beta treatment of normal human nasal epithelial cells (NHNE), lysozyme mRNA expression was determined by RT-PCR. Expressed levels of ERK/p38 kinase were determined by Western blot analysis.
IL-1beta treated NHNEcells had over-expressed lysozyme compared to the control group. Activated ERK/p38 kinase level showed marked increment by treating NHNE with IL-1beta. Lysozyme expression and ERK/p38 kinase levels decreased when inhibitors of ERK/p38 MAP kinases were added to the IL-1beta treated cells. Finally, expression of lysozyme and activated level of ERK/p38 MAP kinases decreased in a dominant-negative cell line even when treated with IL-1beta.
From these results, we concluded that IL-1beta induces over-expression of lysozyme via ERK/p38 MAP kinase signaling pathways in airway epithelial cells.


IL-1beta; Lysozyme; ERK; p38 MAP kinase; Normal human nasal epithelial cells
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