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How Do Innate Immune Cells Contribute to Airway Remodeling in COPD Progression?

Authors Bu T, Wang LF, Yin YQ

Received 17 October 2019

Accepted for publication 19 December 2019

Published 10 January 2020 Volume 2020:15 Pages 107—116

DOI https://doi.org/10.2147/COPD.S235054

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Prof. Dr. Chunxue Bai


Tegeleqi Bu, Li Fang Wang, Yi Qing Yin

Department of Anesthesiology, China-Japan Friendship Hospital, Beijing, People’s Republic of China

Correspondence: Yi Qing Yin
Department of Anesthesiology, China-Japan Friendship Hospital, Ying Hua East Road No. 2, Chaoyang District, Beijing, People’s Republic of China
Tel +86 135 2126 2509
Email yyq518@sina.com

Abstract: Recently, the therapeutic potential of immune-modulation during the progression of chronic obstructive pulmonary disease (COPD) has been attracting increasing interest. However, chronic inflammatory response has been over-simplified in descriptions of the mechanism of COPD progression. As a form of first-line airway defense, epithelial cells exhibit phenotypic alteration, and participate in epithelial layer disorganization, mucus hypersecretion, and extracellular matrix deposition. Dendritic cells (DCs) exhibit attenuated antigen-presenting capacity in patients with advanced COPD. Immature DCs migrate into small airways, where they promote a pro-inflammatory microenvironment and bacterial colonization. In response to damage-associated molecular patterns (DAMPs) in lung tissue affected by COPD, neutrophils are excessively recruited and activated, where they promote a proteolytic microenvironment and fibrotic repair in small airways. Macrophages exhibit decreased phagocytosis in the large airways, while they demonstrate high pro-inflammatory potential in the small airways, and mediate alveolar destruction and chronic airway inflammation. Natural killer T (NKT) cells, eosinophils, and mast cells also play supplementary roles in COPD progression; however, their cellular activities are not yet entirely clear. Overall, during COPD progression, “exhausted” innate immune responses can be observed in the large airways. On the other hand, the innate immune response is enhanced in the small airways. Approaches that inhibit the inflammatory cascade, chemotaxis, or the activation of inflammatory cells could possibly delay the progression of airway remodeling in COPD, and may thus have potential clinical significance.

Keywords: innate immune cell, airway remodeling, lung immunity, immune tolerance, chronic obstructive pulmonary disease

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