Inflammation, chronic obstructive pulmonary disease and aging

Curr Opin Pulm Med. 2011 Dec:17 Suppl 1:S3-10. doi: 10.1097/01.mcp.0000410742.90463.1f.

Abstract

Purpose of review: Chronic obstructive pulmonary disease (COPD) is characterized by an abnormal persistent inflammatory response to noxious environmental stimuli, particularly cigarette smoke. The determinants of the dysregulated immune responses, which play a role both in the onset and continuation of COPD, are largely unknown. We examined several molecular mechanisms regulating the inflammatory pathway, such as cytokine polymorphisms, miRNA expression, and DNA methylation in COPD and aging, with the aim to provide evidence supporting the view that aging of the immune system may predispose to COPD.

Recent findings: The incidence of COPD increases with age. The pathogenesis of the disease is linked to a chronic inflammation and involves the recruitment and regulation of innate and adaptive immune cells. A chronic systemic inflammation characterizes aging and has been correlated with many diseases, most of them age-related.

Summary: COPD and aging are associated with significant dysregulation of the immune system that leads to a chronic inflammatory response. The similar molecular mechanisms and the common genetic signature shared by COPD and aging suggest that immunosenescence may contribute to the development of COPD.

Publication types

  • Review

MeSH terms

  • Aged
  • Aged, 80 and over
  • Aging* / genetics
  • Aging* / immunology
  • DNA Methylation
  • Female
  • Humans
  • Inflammation / immunology
  • Inflammation / metabolism*
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • Male
  • MicroRNAs / metabolism
  • Polymorphism, Single Nucleotide
  • Pulmonary Disease, Chronic Obstructive / epidemiology
  • Pulmonary Disease, Chronic Obstructive / genetics
  • Pulmonary Disease, Chronic Obstructive / immunology
  • Pulmonary Disease, Chronic Obstructive / metabolism*
  • Smoking / adverse effects*
  • Smoking / epidemiology
  • Smoking / immunology
  • Smoking / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-6
  • Interleukin-8
  • MicroRNAs
  • Tumor Necrosis Factor-alpha