HO-1 inhibits IL-13-induced goblet cell hyperplasia associated with CLCA1 suppression in normal human bronchial epithelial cells

Mucus hypersecretion and goblet cell hyperplasia are common features that characterize asthma. IL-13 increases mucin (MUC) 5AC, the major component of airway mucus, in airway epithelial cells. According to the literature, IL-13 receptor activation leads to STAT6 activation and consequent induction o...

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Veröffentlicht in:International immunopharmacology 2015-12, Vol.29 (2), p.448-453
Hauptverfasser: Mishina, Kei, Shinkai, Masaharu, Shimokawaji, Tadasuke, Nagashima, Akimichi, Hashimoto, Yusuke, Inoue, Yoriko, Inayama, Yoshiaki, Rubin, Bruce K., Ishigatsubo, Yoshiaki, Kaneko, Takeshi
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Sprache:eng
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Zusammenfassung:Mucus hypersecretion and goblet cell hyperplasia are common features that characterize asthma. IL-13 increases mucin (MUC) 5AC, the major component of airway mucus, in airway epithelial cells. According to the literature, IL-13 receptor activation leads to STAT6 activation and consequent induction of chloride channel accessory 1 (CLCA1) gene expression, associated with the induction of MUC5AC. Heme oxygenase-1 (HO-1) is an enzyme that catalyzes oxidation of heme to biliverdin, and has anti-inflammatory and anti-oxidant properties. We examined the effects of HO-1 on mucin production and goblet cell hyperplasia induced by IL-13. Moreover, we assessed the cell signaling intermediates that appear to be responsible for mucin production. Normal human bronchial epithelial (NHBE) cells were grown at air liquid interface (ALI) in the presence or absence of IL-13 and hemin, a HO-1 inducer, for 14days. Protein concentration was analyzed using ELISA, and mRNA expression was examined by real-time PCR. Histochemical analysis was performed using HE staining, and Western blotting was performed to evaluate signaling transduction pathway. Hemin (4μM) significantly increased HO-1 protein expression (p
ISSN:1567-5769
1878-1705
DOI:10.1016/j.intimp.2015.10.016