Innate immunity and chronic obstructive pulmonary disease: a mini-review. Review uri icon

Overview

MeSH

  • Aging
  • Antioxidants
  • Dendritic Cells
  • Disease Progression
  • Humans
  • Immunomodulation
  • Inflammation
  • Killer Cells, Natural
  • Lung
  • Macrophages, Alveolar
  • Neutrophils
  • Respiratory Mucosa
  • Respiratory Tract Infections
  • Smoking

MeSH Major

  • Immunity, Innate
  • Pulmonary Disease, Chronic Obstructive

abstract

  • Chronic obstructive pulmonary disease (COPD), a major smoking-associated lung disorder characterized by progressive irreversible airflow limitation, affects >200 million people worldwide. Individuals with COPD have increased susceptibility to respiratory infections, resulting in exacerbations of the disease. A growing body of evidence indicates that multiple host defense mechanisms, such as those provided by the airway epithelial barrier and innate immune cells, including alveolar macrophages, neutrophils, dendritic cells and natural killer cells, are broadly suppressed in COPD in a smoking-dependent manner. Inactivation of the innate immune system observed in COPD smokers is remarkably similar to the immunosenescence phenotype associated with aging. As a consequence of defective innate immune defense, the lungs of COPD smokers are frequently colonized with pathogens and commonly develop bacterial and viral infections, which cause secondary inflammation, a major driver of the disease progression. In this review, we summarize the evidence from human studies related to disordering of the innate immune system in COPD, discuss possible relationships between those changes and aging, and provide insights into potential therapeutic strategies aimed at the prevention of COPD progression via normalization of the disordered innate immune mechanisms. © 2013 S. Karger AG, Basel.

publication date

  • 2013

has subject area

  • Aging
  • Antioxidants
  • Dendritic Cells
  • Disease Progression
  • Humans
  • Immunity, Innate
  • Immunomodulation
  • Inflammation
  • Killer Cells, Natural
  • Lung
  • Macrophages, Alveolar
  • Neutrophils
  • Pulmonary Disease, Chronic Obstructive
  • Respiratory Mucosa
  • Respiratory Tract Infections
  • Smoking

Research

keywords

  • Journal Article
  • Review

Identity

Language

  • eng

PubMed Central ID

  • PMC3833667

Digital Object Identifier (DOI)

  • 10.1159/000354173

PubMed ID

  • 24008598

Additional Document Info

start page

  • 481

end page

  • 489

volume

  • 59

number

  • 6