P38 MAP‐Kinase Pathway Is Involved in the Production of CLC‐3 in Nasal Epithelial Cells With Allergic Rhinitis Induced by Interleukin‐4

Abstract

The objective of this study was to evaluate the role of p38 MAP-kinase (MAPK) pathway on CLC-3 expression after interleukin-4 (IL-4) induction in primary cultured human nasal epithelial cells (HNECs) from patients with allergic rhinitis (AR). Cultured HNECs from five patients with AR were treated with IL-4 (20 ng/mL) with or without SB203580, a selective inhibitor of p38 MAPK, at different concentrations and durations. CLC-3 was detected in HNECs by immunohistochemistry and real-time quantitative reverse transcription-polymerase chain reaction. p38 MAPK and phosphorylated p38 MAPK (pp38 MAPK) was examined by Western blotting. After exposure to SB203580, CLC-3 expression induced by IL-4 was downregulated in HNECs in a concentration and time-dependent manner. This downregulation was associated with a decrease in pp38 MAPK. These results confirmed that IL-4 can induce CLC-3 production in HNECs with AR through a p38 MAPK-dependent pathway. Inhibitors of p38 MAPK may become an important strategy for the treatment of AR.