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Protection against STING-associated lung disease

ABSTRACT: Transferrable protection by gut microbes against STING-associated lung disease

PROVIDER: PRJEB42379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR5167990_1.fastq.gz	Fastqsanger.gz
	ERR5167990_2.fastq.gz	Fastqsanger.gz
	ERR5168000_1.fastq.gz	Fastqsanger.gz
	ERR5168000_2.fastq.gz	Fastqsanger.gz
	ERR5168010_1.fastq.gz	Fastqsanger.gz

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Transferrable protection by gut microbes against STING-associated lung disease.

Project description:STING modulates immunity by responding to bacterial and endogenous cyclic dinucleotides (CDNs). Humans and mice with STING gain-of-function mutations develop a syndrome known as STING-associated vasculopathy with onset in infancy (SAVI), which is characterized by inflammatory or fibrosing lung disease. We hypothesized that hyperresponsiveness of gain-of-function STING to bacterial CDNs might explain autoinflammatory lung disease in SAVI mice. We report that depletion of gut microbes with oral antibiotics (vancomycin, neomycin, and ampicillin [VNA]) nearly eliminates lung disease in SAVI mice, implying that gut microbes might promote STING-associated autoinflammation. However, we show that germ-free SAVI mice still develop severe autoinflammatory disease and that transferring gut microbiota from antibiotics-treated mice to germ-free animals eliminates lung inflammation. Depletion of anaerobes with metronidazole abolishes the protective effect of the VNA antibiotics cocktail, and recolonization with the metronidazole-sensitive anaerobe Bacteroides thetaiotaomicron prevents disease, confirming a protective role of a metronidazole-sensitive microbe in a model of SAVI.

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