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Type I IFN Expression is Stimulated by Cytosolic MtDNA Released from Pneumolysin-Damaged Mitochondria Via the STING Signaling Pathway in Macrophages.

著者 Hu X , Peng X , Lu C , Zhang X , Gan L , Gao Y , Yang S , Xu W , Wang J , Yin Y , Wang H
FEBS J.2019 Jul 17 ; ():.
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Pneumolysin (Ply), a major virulence factor of Streptococcus pneumoniae (S. pn), affects the immunity of host cells during infection. It has been reported that Ply is involved in S. pn standard strain D39-induced interferon-β (IFN-β) expression, however, other findings suggest that recombinant Ply protein is incapable of triggering IFN-β expression. Here, we demonstrated that purified Ply was capable of initiating oxidative damage to mitochondria, resulting in the subsequent release of mitochondrial deoxyribonucleic acid (mtDNA), which mediated IFN-β expression in macrophages. Importantly, we determined that IFN-β expression was regulated by stimulator of interferon genes (STING) signaling in response to Ply. In conclusion, our study identified that IFN-β production was triggered by Ply in macrophages and mtDNA released from Ply-damaged mitochondria mediated this process, through the STING pathway. This is a novel mechanism by which S. pn modulates type I IFN response in macrophages. This article is protected by copyright. All rights reserved.
PMID: 31315154 [PubMed - as supplied by publisher]
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