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Cited by 106Chronic Obstructive Pulmonary Disease (COPD) ResearchAsthma and respiratory diseasesSmoking Behavior and Cessation

The Aging Immune System and Its Relationship to the Development of Chronic Obstructive Pulmonary Disease

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Sharma, Gulshan, Hanania, Nicola A., Shim, Y. Michael·2009·Proceedings of the American Thoracic Society
DOI 10.1513/pats.200904-022rmPMC PMC5820858
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Abstract

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease of the lungs that usually manifests late in life. Physiologic and immunologic changes that occur in COPD often mimic changes seen in the aging lung. This has led some to characterize COPD as an “accelerated aging phenotype.” At the molecular level, COPD and aging share common mechanisms and are associated with significant dysregulation of the immune systems. Aging and COPD are characterized by increases in proinflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α, which are implicated in aging-related inflammatory diseases and correlate with degree of obstruction in COPD. There is an age-dependent decline in naïve T cells with oligoclonal expansion of CD8+ CD28null T cells from chronic antigenic stimulation. The increase in CD8+ CD28 null T regulatory cells inhibits antigen-specific CD4+ T cell responses, leading to a decline in adaptive immune response. To compensate for the decline in the adaptive immune function there is a paradoxical up-regulation of innate immune system resulting in a proinflammatory state. The dysregulated adaptive immune system with activated innate immune responses seen with aging results in recruitment and retention of neutrophils, macrophages, and CD4+ and CD8+ T cells in the lungs of smokers with COPD. Once the inflammation is triggered, there is a self-perpetuating cascade of inflammation and lung parenchymal damage. This review will focus on how the aging immune system may contribute to COPD development later in life in susceptible individuals.

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Crossref · 10.1513/pats.200904-022rm

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108 of 108 references verified0 citation errors · 0 not checkable

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  • Due to changes in lung function and anatomy as well as lung antioxidant defenses, the aged lung is more susceptible to environmental exposure-induced injury.

    “Due to changes in lung function and anatomy as well as lung antioxidant defenses, the aged lung is more susceptible to environmental exposure–induced injury (19, 86).”

    From Aging and Lung Disease (2020) · cites this paper as [86]

  • Age-associated immunosenescence and cellular senescence in response to exposure to cigarette smoke can greatly impact COPD pathogenesis.

    “Age-associated immunosenescence and cellular senescence in response to exposure to cigarette smoke can greatly impact COPD pathogenesis (3, 19, 86).”

    From Aging and Lung Disease (2020) · cites this paper as [86]

  • Acute exacerbations of COPD (AECOPD) are common in patients with severe and very severe COPD and are characterized by increased dyspnea, purulence, and augmented sputum volume.

    “Acute exacerbations of COPD (AECOPD) are common in patients with severe and very severe COPD and are characterized by increased dyspnea, purulence, and augmented sputum volume (86, 137).”

    From Aging and Lung Disease (2020) · cites this paper as [86]

  • An age-dependent increase in cytotoxic CD8+ and memory CD4+ T cells in the airways of COPD patients may further disease progression.

    “An age-dependent increase in cytotoxic CD8+ and memory CD4+ T cells in the airways of COPD patients may further disease progression (86, 130, 132).”

    From Aging and Lung Disease (2020) · cites this paper as [86]

  • Macrophages, which can produce multiple proinflammatory cytokines and secrete MMPs, are the most abundant cell type in the BAL fluid of COPD patients, and increased numbers correlate with disease severity.

    “Specifically, macrophages, which can produce multiple proinflammatory cytokines and secrete MMPs, are the most abundant cell type in the BAL fluid of COPD patients, and increased numbers correlate with disease severity (85, 86, 104).”

    From Aging and Lung Disease (2020) · cites this paper as [86]

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Authors
Sharma, G., Hanania, N. A., & Shim, Y. M.
Affiliations
  • The University of Texas Medical Branch at Galveston (US)
  • Baylor College of Medicine (US)
  • University of Virginia (US)
Corresponding author
Sharma, Gulshan
ORCID
Venue
Proceedings of the American Thoracic Society
Publisher
Oxford University Press (OUP)
Published
2009-12-01
Volume
6
Issue
7
Pages
573-580
ISSN
  • 1546-3222 (ISSN-L)
  • 1943-5665
DOI
10.1513/pats.200904-022rm
PMC
PMC5820858
OpenAlex
W2158912859
Cited by
105
References
106
Citations by year
2026: 5 · 2025: 4 · 2024: 10 · 2023: 4 · 2022: 10 · 2021: 5 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 7 · 2016: 4 · 2015: 9 · 2014: 7 · 2013: 11 · 2012: 8
FWCI
0.99
Type
journal article
Language
en
Open access
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • Proceedings of the American Thoracic Society (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (K08HL091127)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
Keywords
chronic obstructive pulmonary disease, immunosenescence, inflammatory cytokines, interleukin-6, TNF-α, CD8+CD28- T cells, regulatory T cells, innate immune activation, neutrophil recruitment, macrophages, smoking, lung inflammation
MeSH terms
Aging, Humans, Immunity, Tumor Necrosis Factor-alpha, Interleukin-6, Pulmonary Disease, Chronic Obstructive

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