Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice. Academic Article uri icon

Overview

abstract

  • Cigarette smoke exposure is a leading cause of chronic obstructive pulmonary disease (COPD), a major health issue characterized by airway inflammation with fibrosis and emphysema. Here we demonstrate that acute exposure to cigarette smoke causes respiratory barrier damage with the release of self-dsDNA in mice. This triggers the DNA sensor cGAS (cyclic GMP-AMP synthase) and stimulator of interferon genes (STING), driving type I interferon (IFN I) dependent lung inflammation, which are attenuated in cGAS, STING or type I interferon receptor (IFNAR) deficient mice. Therefore, we demonstrate a critical role of self-dsDNA release and of the cGAS-STING-type I interferon pathway upon cigarette smoke-induced damage, which may lead to therapeutic targets in COPD.

publication date

  • October 16, 2019

Research

keywords

  • DNA
  • Membrane Proteins
  • Nucleotidyltransferases
  • Pneumonia
  • Pulmonary Emphysema
  • Receptor, Interferon alpha-beta
  • Tobacco Smoke Pollution

Identity

PubMed Central ID

  • PMC6795997

Scopus Document Identifier

  • 85073409519

Digital Object Identifier (DOI)

  • 10.1038/s41598-019-51427-y

PubMed ID

  • 31619733

Additional Document Info

volume

  • 9

issue

  • 1