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Oleuropein inhibits IL‐4‐induced epithelial‐mesenchymal transition in airway epithelial cells
Author(s) -
Gong JuHyun,
Kang YoungHee
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.586.8
Subject(s) - eotaxin , oleuropein , epithelial–mesenchymal transition , chemokine , airway , immunology , ccl20 , inflammation , medicine , chemistry , chemokine receptor , downregulation and upregulation , biochemistry , gene , antioxidant , surgery
Allergic asthma is characterized by airway inflammation in response to antigen exposure, resulting in airway remodeling and lung dysfunction. Epithelial‐mesenchymal transition (EMT) may play a role in airway remodeling through the acquisition of a mesenchymal phenotype in the airway epithelium.We elucidated inhibitory effects of oleuropein, a type of phenolic compound with anti‐inflammatory activity, on interleukin (IL)‐4 or eotaxin‐induced airway remodeling in human bronchial airway epithelial BEAS‐2B cells.IL‐4 markedly induced epithelial eotaxin‐1 and chemokine receptor CCR3 expression. Nontoxic oleuropein at 蠄20 μM significantly attenuated the IL‐4‐elevated expression of eotaxin‐1 and CCR3 in BEAS‐2B cells for 72 h. Additionally, 1‐20 μM oleuropein dose‐dependently inhibited the IL‐4 and eotaxin‐induced production of α‐smooth muscle actin (α‐SMA). These results demonstrate that dietary oleuropein suppressed IL‐4 and eotaxin‐1 promoted bronchial epithelial EMT leading to airway remodeling with concurrent loss of E‐cadherin and induction of α‐SMA. Therefore, oleuropein may be a potential therapeutic agent targeting asthmatic airway constriction.