Inflammasome signaling in pathogenesis of lung diseases

Curr Pharm Des. 2012;18(16):2320-8. doi: 10.2174/138161212800166077.

Abstract

Asthma and Chronic Obstructive Pulmonary Disease (COPD) are two important lung and airways diseases which affect the lives of ∼500 million people worldwide. Asthma is a heterogeneous disease that is broadly defined as a clinical syndrome characterized by altered lung function, mucus hypersecretion, peribronchial inflammation and hyperresponsiveness In contrast, the effect of inhalation of toxic particles and gases on the innate and adaptive inflammatory immune systems underlie the pathogenesis of COPD. In the last decade, knowledge concerning the pathophysiologic mechanisms underlying asthma and COPD has risen tremendously and current dogma suggests that the pathogenesis of both diseases is driven by the chronic inflammation present in the airways of these patients. Thus, understanding the mechanisms for the persistence of inflammation may lead to new therapeutic approaches. In this review, we provide an overview of the main signal transduction pathways implicated in asthma and COPD pathophysiology focusing on inflammasome signaling in various cells types which result in altered inflammatory mediator expression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Asthma / etiology
  • Asthma / immunology
  • Asthma / metabolism
  • Chromatin / metabolism
  • Humans
  • Inflammasomes / metabolism*
  • Inflammation Mediators / metabolism
  • Lung Diseases / etiology*
  • Lung Diseases / immunology
  • Lung Diseases / metabolism
  • NF-kappa B / metabolism
  • Pulmonary Disease, Chronic Obstructive / etiology
  • Pulmonary Disease, Chronic Obstructive / immunology
  • Pulmonary Disease, Chronic Obstructive / metabolism
  • Signal Transduction*
  • Toll-Like Receptors / metabolism

Substances

  • Chromatin
  • Inflammasomes
  • Inflammation Mediators
  • NF-kappa B
  • Toll-Like Receptors