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Authors Zeng ZL, Li M, Chen JK, Li QH, Ning Q, Zhao JP, Xu YJ, Xie JG, Yu J
Received 8 August 2017
Accepted for publication 9 October 2017
Published 28 February 2018 Volume 2018:13 Pages 703—715
DOI https://doi.org/10.2147/COPD.S148595
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Colin Mak
Peer reviewer comments 2
Editor who approved publication: Prof. Dr. Chunxue Bai
Background: Chronic
obstructive pulmonary disease (COPD) is a common inflammatory lung disease
characterized by inflammatory cells activation and production of inflammatory
mediators. Methyl-CpG-binding domain protein 2 (MBD2) plays an important role
in diverse immunological disorders by regulating immune cell functions, such as
differentiation and mediator secretion. However, the role of MBD2 in COPD
remains unknown.
Methods: MBD2 protein expression in lung tissues of patients with COPD and
cigarette smoke (CS)-exposed mice were evaluated by Western blot and
immunohistochemistry. The role of MBD2 in cigarette smoke extract
(CSE)-induction of inflammatory mediator expression in the human bronchial epithelial
(HBE) cell line was assessed by silencing MBD2 expression in vitro. The
involvement of signaling pathways in mediation of inflammation was tested with
signaling inhibitors.
Results: Compared with controls, MBD2 expression was distinctly reduced in
the bronchial epithelium of both patients with COPD and CS-exposed mice.
Moreover, MBD2 expression was decreased in HBE after CSE stimulation in vitro.
Moreover, MBD2 knockdown enhanced interleukin (IL)-6 and IL-8 expression in HBE
in the presence and absence of CSE treatment by the ERK signaling pathway.
Conclusion: MBD2 protein expression was reduced in the airway epithelium of COPD. In
HBE, this reduced expression was associated with increased levels of IL-6 and
IL-8 mediated by the ERK pathway. These results suggest that MBD2 could
contribute to chronic airway inflammation in COPD.
Keywords: chronic obstructive pulmonary disease, methyl-CpG-binding domain
protein 2, airway inflammation