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Journal of Immunology Research
Volume 2018, Article ID 2349045, 19 pages
Review Article

Dysregulated Functions of Lung Macrophage Populations in COPD

1Genomics & Immunoregulation, Life and Medical Sciences Institute (LIMES), Carl-Troll-Str. 31, 53115 Bonn, Germany
2Platform for Single Cell Genomics and Epigenomics, German Center for Neurodegenerative Diseases and University of Bonn, Sigmund-Freud-Str. 27, 53175 Bonn, Germany

Correspondence should be addressed to Theodore S. Kapellos; ed.nnob-inu@ollepakt and Joachim L. Schultze; ed.nnob-inu@eztluhcs.j

Received 30 July 2017; Accepted 29 November 2017; Published 18 February 2018

Academic Editor: Ethan M. Shevach

Copyright © 2018 Theodore S. Kapellos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic obstructive pulmonary disease (COPD) is a diverse respiratory disease characterised by bronchiolitis, small airway obstruction, and emphysema. Innate immune cells play a pivotal role in the disease’s progression, and in particular, lung macrophages exploit their prevalence and strategic localisation to orchestrate immune responses. To date, alveolar and interstitial resident macrophages as well as blood monocytes have been described in the lungs of patients with COPD contributing to disease pathology by changes in their functional repertoire. In this review, we summarise recent evidence from human studies and work with animal models of COPD with regard to altered functions of each of these myeloid cell populations. We primarily focus on the dysregulated capacity of alveolar macrophages to secrete proinflammatory mediators and proteases, induce oxidative stress, engulf microbes and apoptotic cells, and express surface and intracellular markers in patients with COPD. In addition, we discuss the differences in the responses between alveolar macrophages and interstitial macrophages/monocytes in the disease and propose how the field should advance to better understand the implications of lung macrophage functions in COPD.