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Review
. 2019 May;60(5):407-413.
doi: 10.3349/ymj.2019.60.5.407.

COPD as a Disease of Immunosenescence

Won Kyung Cho  1 , Chun Geun Lee  2 , Lark Kyun Kim  3
Affiliations
Review

COPD as a Disease of Immunosenescence

Won Kyung Cho et al. Yonsei Med J. 2019 May.

Abstract

Although chronic obstructive pulmonary disease (COPD) is regarded as a chronic inflammatory lung disease, the disease mechanism is still not known. Intriguingly, aging lungs are quite similar to COPD-affected lungs in many ways, and COPD has been viewed as a disease of accelerated premature aging of the lungs. In this paper, based on a literature review, we would like to propose immunosenescence, age-associated decline in immunity, as a critical mechanism for the development of COPD. Immunosenescence can cause a low-grade, systemic inflammation described as inflammaging. This inflammaging may be directly involved in the COPD pathogenesis. The potential contributors to the development of inflammaging in the lungs possibly leading to COPD are discussed in the review paper. A notable fact about COPD is that only 15% to 20% of smokers develop clinically significant COPD. Given that there is a substantial inter-individual variation in inflammaging susceptibility, which is genetically determined and significantly affected by the history of the individual's exposure to pathogens, immunosenescence and inflammaging may also provide the answer for this unexpectedly low susceptibility of smokers to clinically significant COPD.

Keywords: COPD; aging; immunosenescence; inflammaging; inflammation.

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Conflict of interest statement

The authors have no potential conflicts of interest to disclose.

Figures

Fig. 1
Fig. 1. Causes and risk factors for COPD. Besides exposure to noxious particles or gases, host factors determine the susceptibility of individuals to develop COPD. COPD, chronic obstructive pulmonary disease.
Fig. 2
Fig. 2. Inflammaging: a new mechanism of age-related disease. Low-grade inflammation called inflammaging during the ageing process may contribute to the pathogenesis of most age-related diseases. SLPI, secretory leukocyte protease inhibitor; PAMP, pathogen-associated molecular pattern; DAMP, damage-associated molecular pattern; TLR, Toll-like receptor; NLR, NOD-like receptor; SASP, senescence-associated secretory phenotype.
Fig. 3
Fig. 3. Overview of immune hypotheses on COPD. Different levels of inflammaging caused by immunosenescence determine the susceptibility of individuals to COPD. COPD, chronic obstructive pulmonary disease.
See this image and copyright information in PMC

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