Journal
IMMUNITY
Volume 55, Issue 5, Pages 847-+Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2022.04.006
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Funding
- Stockholm University
- Laboratory for Molecular Infection Medicine Sweden (MIMS)
- Swedish Research Council [2015-02857, 2016-00890, 2018-02914, 2015-03007, 2015-06824, 2019-01720, 2016-06598]
- Ume University (Faculty of Science and Technology)
- Kempestiftelserna [SMK-1858.2]
- Ake Wibergs stiftelse [M19-0314]
- Knut and Alice Wallenberg Foundation
- University of Gothenburg
- Swedish Cancer Foundation [CAN 2017/421, 2017/419]
- Swedish Research Council [2018-02914, 2015-06824, 2015-02857, 2016-00890] Funding Source: Swedish Research Council
- Vinnova [2018-02914] Funding Source: Vinnova
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This study revealed the modulation of systemic immunity and response to viral infection by gut commensals. Peripheral cGAS-STING activation plays a crucial role in promoting host resistance to systemic viral infections.
The microbiota are vital for immune homeostasis and provide a competitive barrier to bacterial and fungal pathogens. Here, we investigated how gut commensals modulate systemic immunity and response to viral infection. Antibiotic suppression of the gut microbiota reduced systemic tonic type I interferon (IFN-I) and antiviral priming. The microbiota-driven tonic IFN-I-response was dependent on cGAS-STING but not on TLR signaling or direct host-bacteria interactions. Instead, membrane vesicles (MVs) from extracellular bacteria activated the cGAS-STING-IFN-I axis by delivering bacterial DNA into distal host cells. DNA-containing MVs from the gut microbiota were found in circulation and promoted the clearance of both DNA (herpes simplex virus type 1) and RNA (vesicular stomatitis virus) viruses in a cGAS-dependent manner. In summary, this study establishes an important role for the microbiota in peripheral cGAS-STING activation, which promotes host resistance to systemic viral infections. Moreover, it uncovers an underappreciated risk of antibiotic use during viral infections.
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