Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice

Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice

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 o...

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Bibliographic Details
Main Authors: Mégane Nascimento, Aurélie Gombault, Norinne Lacerda-Queiroz, Corinne Panek, Florence Savigny, Malak Sbeity, Manon Bourinet, Marc Le Bert, Nicolas Riteau, Bernhard Ryffel, Valérie F. J. Quesniaux, Isabelle Couillin
Format: Article
Language:English
Published: Nature Publishing Group 2019-10-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-019-51427-y
Description
Summary: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.
ISSN:2045-2322

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