Cells, mediators and Toll-like receptors in COPD

Eur J Pharmacol. 2008 May 13;585(2-3):346-53. doi: 10.1016/j.ejphar.2008.03.009. Epub 2008 Mar 18.

Abstract

Chronic obstructive pulmonary disease (COPD) is a global health problem. Being a progressive disease characterized by inflammation, it deteriorates pulmonary functioning. Research has focused on airway inflammation, oxidative stress, and remodelling of the airways. Macrophages, neutrophils and T cells are thought to be important key players. A number of new research topics received special attention in the last years. The combined use of inhaled corticosteroids and long-acting beta(2)-adrenoceptor agonists produces better control of symptoms and lung function than that of the use of either compound alone. Furthermore, collagen breakdown products might be involved in the recruitment and activation of inflammatory cells by which the process of airway remodelling becomes self-sustaining. Also, TLR (Toll-like receptor)-based signalling pathways seem to be involved in the pathogenesis of COPD. These new findings may lead to new therapeutic strategies to stop the process of inflammation and self-destruction in the airways of COPD patients.

Publication types

  • Review

MeSH terms

  • Adrenal Cortex Hormones / therapeutic use
  • Adrenergic beta-Agonists / therapeutic use
  • Animals
  • Chemokines / physiology
  • Cytokines / physiology
  • Epithelial Cells / physiology
  • Humans
  • Inflammation Mediators / physiology
  • Leukocytes / physiology
  • Pulmonary Disease, Chronic Obstructive / drug therapy
  • Pulmonary Disease, Chronic Obstructive / etiology
  • Pulmonary Disease, Chronic Obstructive / pathology*
  • Pulmonary Disease, Chronic Obstructive / physiopathology*
  • Toll-Like Receptors / drug effects
  • Toll-Like Receptors / physiology*

Substances

  • Adrenal Cortex Hormones
  • Adrenergic beta-Agonists
  • Chemokines
  • Cytokines
  • Inflammation Mediators
  • Toll-Like Receptors