Mitochondrial Regulation of Inflammasome Activation in Chronic Obstructive Pulmonary Disease

J Innate Immun. 2016;8(2):121-8. doi: 10.1159/000441299. Epub 2015 Nov 5.

Abstract

Chronic obstructive pulmonary disease (COPD) is characterized by enhanced chronic airway and lung inflammatory responses to noxious particles or gases. It is a major unmet medical need worldwide, and in Western society is strongly associated with exposure to cigarette smoke (CS). CS-induced inflammation is believed to be a key immune driver in the pathogenesis of COPD. Since the concept of inflammasomes was first introduced nearly a decade ago, these have been increasingly recognized as a central player in innate immune and inflammatory responses. In addition, studies have emerged demonstrating that mitochondrial innate immune signaling plays an important role in CS-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. Here, recent discoveries about inflammasome activation and mitochondrial biology and their role in COPD pathogenesis are reviewed. In addition, the current limitations of our understanding of this theme and future research directions are discussed.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Humans
  • Immunity, Innate*
  • Inflammasomes / immunology*
  • Inflammation / immunology
  • Inflammation / pathology
  • Mitochondria / immunology*
  • Mitochondria / pathology
  • Pulmonary Disease, Chronic Obstructive / immunology*
  • Pulmonary Disease, Chronic Obstructive / pathology
  • Signal Transduction / immunology*
  • Smoking / immunology
  • Smoking / pathology

Substances

  • Inflammasomes