Document Type

Article

Publication Date

1-1-2026

Keywords

JMG, Animals, Nucleotidyltransferases, Leptospira interrogans, Interferon Type I, Leptospirosis, Mice, Membrane Proteins, Mice, Knockout, Humans, Kidney, Signal Transduction, Mice, Inbred C57BL, Immunity, Innate, Macrophages, Receptor, Interferon alpha-beta, STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase

JAX Source

PLoS Pathog. 2026;22(1):e1013250.

ISSN

1553-7374

PMID

41499635

DOI

https://doi.org/10.1371/journal.ppat.1013250

Abstract

Leptospira interrogans is the major causative agent of leptospirosis. Humans, canines and agricultural animals are susceptible to Leptospira species and can develop fulminant disease. Rodents serve as reservoir hosts in which the bacteria colonize the renal tubules and are excreted in the urine. The host immune response to Leptospira spp. remains poorly defined. We show that L. interrogans induces a robust type I interferon (IFN) response in human and murine macrophages that is dependent on the cytosolic dsDNA sensor Cyclic GMP-AMP Synthase (cGAS) and the Stimulator of IFN Genes (STING) signaling pathway. Further, we show that mice deficient in the IFNα/β receptor subunit 1 (IFNAR1) or STING had higher bacterial burdens and increased renal colonization following infection in vivo suggesting that cGAS-STING-driven type I IFN is required for the host defense against L. interrogans. These findings demonstrate the significance of cGAS-STING- dependent type I IFN signaling in mammalian innate immune responses to L. interrogans.

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