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.