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Expression of heme oxygenase‐1 in eosinophilic and non‐eosinophilic chronic rhinosinusitis with nasal polyps: modulation by cytokines
Author(s) -
Yu Zhijian,
Wang Yu,
Zhang Jia,
Li Lei,
Wu Xingmei,
Ma Renqiang,
Han Miaomiao,
Xu Geng,
Wen Weiping,
Li Huabin
Publication year - 2015
Publication title -
international forum of allergy and rhinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.503
H-Index - 46
eISSN - 2042-6984
pISSN - 2042-6976
DOI - 10.1002/alr.21530
Subject(s) - nasal polyps , medicine , heme oxygenase , eosinophilic , western blot , messenger rna , interleukin , oxidative stress , immunology , proinflammatory cytokine , immunohistochemistry , pathology , cytokine , inflammation , heme , biology , gene , enzyme , biochemistry
Background Oxidative stress is characteristic of chronic airway inflammatory diseases such as asthma, chronic obstructive pulmonary disease and chronic rhinosinusitis with nasal polyps (CRSwNP). Heme oxygenase (HO)‐1 has been proposed to be a cytoprotective enzyme against oxidative stress in CRSwNP. However, the expression and regulation of HO‐1 in eosinophilic CRSwNP (ECRS) and non‐eosinophilic CRSwNP (non‐ECRS) subsets has not been well documented. Methods Nasal polyps and uncinate process tissues were enrolled from 40 CRSwNP patients (ECRS, 17; non‐ECRS, 23) and 20 control subjects, respectively. The messenger RNA (mRNA) and protein expression of HO‐1 was examined using qRT‐PCR, immunohistochemistry, and Western blot staining. Moreover, the stimulatory effects of several cytokines (interferon γ [IFN‐γ], interleukin [IL]‐5, and IL‐13, etc.) on HO‐1 mRNA expression in cultured nasal explants were evaluated. Results The mRNA and protein expression of HO‐1 was significantly increased in polyp tissues compared with healthy controls ( p < 0.05), and the non‐ECRS subset showed significantly increased HO‐1 expression compared with the ECRS subset ( p < 0.05). Moreover, in cultured nasal explant, HO‐1 mRNA was significantly upregulated in the presence of IFN‐γ, IL‐27, IL‐5, IL‐13, and IL‐17A, but was significantly inhibited by transforming growth factor β1 (TGF‐β1) ( p < 0.05). Conclusion Our findings indicate that HO‐1 was differentially expressed and regulated in ECRS and non‐ECRS patients.