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cGAS-STING dependent type I IFN reduces Leptospira interrogans renal colonization in mice
Suman Gupta1,2, James Matsunaga3,4, Bridget Ratitong1,2
1Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, United States of America.
Plos Pathogens
|January 7, 2026
Summary
Leptospira interrogans infection triggers a type I interferon response mediated by cGAS-STING signaling. This pathway is crucial for controlling bacterial load and preventing kidney colonization in mammals.
Area of Science:
- Infectious Diseases
- Immunology
- Microbiology
Background:
- Leptospira interrogans causes leptospirosis in humans and animals.
- Rodents are key reservoirs, excreting bacteria in urine.
- The host immune response to Leptospira is not well understood.
Purpose of the Study:
- To investigate the innate immune response to L. interrogans.
- To identify the signaling pathways involved in host defense.
Main Methods:
- Studied type I interferon (IFN) response in human and murine macrophages.
- Utilized knockout mice deficient in IFNAR1 or STING.
- Assessed bacterial burden and renal colonization in vivo.
Main Results:
- L. interrogans induced a type I IFN response dependent on cGAS and STING.
- Mice lacking IFNAR1 or STING showed increased bacterial burdens.
- Impaired cGAS-STING signaling led to higher renal colonization.
Conclusions:
- The cGAS-STING pathway is essential for innate immunity against L. interrogans.
- Type I IFN signaling plays a critical role in controlling leptospirosis.
- This study elucidates a key mammalian defense mechanism against bacterial infection.
