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P38 MAP‐Kinase Pathway Is Involved in the Production of CLC‐3 in Nasal Epithelial Cells With Allergic Rhinitis Induced by Interleukin‐4
Author(s) -
Han Demin,
Zhou Bing,
Cheng Lei,
Oh Yun,
Li Huabin
Publication year - 2006
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/01.mlg.0000236078.81313.c8
Subject(s) - mapk/erk pathway , p38 mitogen activated protein kinases , downregulation and upregulation , medicine , blot , kinase , immunohistochemistry , mitogen activated protein kinase , interleukin , immunology , cancer research , microbiology and biotechnology , chemistry , biology , cytokine , gene , biochemistry
Objective: 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). Methods: 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. Results: 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. Conclusion: 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.