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 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.
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https://hal.archives-ouvertes.fr/hal-02354641
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Submitted on : Thursday, November 7, 2019 - 7:39:54 PM
Last modification on : Friday, November 8, 2019 - 12:15:43 PM

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Mégane Nascimento, Aurélie Gombault, Norinne Lacerda-Queiroz, Corinne Panek, Florence Savigny, et al.. Self-DNA release and STING-dependent sensing drives inflammation to cigarette smoke in mice. Scientific Reports, Nature Publishing Group, 2019, 9 (1), ⟨10.1038/s41598-019-51427-y⟩. ⟨hal-02354641⟩

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