The Pathology of Chronic Obstructive Pulmonary Disease

James C. Hogg*, Wim Timens

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

604 Citations (Scopus)

Abstract

The pathogenesis of chronic obstructive pulmonary disease (COPD) is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although tobacco smoking is the primary cause of this inhalation injury, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue-repair and -remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The common form of emphysema observed in smokers begins in the respiratory bronchioles near the thickened and narrowed small bronchioles that become the major site of obstruction in COPD. The mechanism(s) that allow small airways to thicken in such close proximity to lung tissue undergoing emphysematous destruction remains a puzzle that needs to be solved.

Original languageEnglish
Pages (from-to)435-459
Number of pages25
JournalAnnual review of pathology-Mechanisms of disease
Volume4
DOIs
Publication statusPublished - 2009

Keywords

  • emphysema
  • remodeling
  • smoking
  • tissue repair
  • CHEMOKINE RECEPTOR CXCR3
  • AIRWAY EPITHELIAL-CELLS
  • LYMPHOID-TISSUE BALT
  • HUMAN BONE-MARROW
  • CIGARETTE-SMOKE
  • CHRONIC-BRONCHITIS
  • PERIPHERAL AIRWAYS
  • LUNG-DISEASE
  • ALVEOLAR MACROPHAGES
  • LEUKOCYTE COUNT

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