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Induction of antiviral Interferon-Stimulated Genes (ISGs) by neuronal STING promotes the resolution of pain

ABSTRACT: Nociceptive neurons respond to inflammation, initiating protective reflexes and alerting the host. Here we found that TRPV1 nociceptors express and activate the cytosolic DNA-sensing protein Stimulator of Interferon Genes (STING) in response to inflammation. Neuronal activation of STING promotes signaling through TBK1 and triggers a Type I interferon (IFN-I) response. The absence of STING led to heightened pain responses to chemical irritants or heat. In contrast, mice expressing a nociceptor-specific gain-of-function mutation in STING exhibited an IFN gene signature that reduced nociceptor excitability and inflammatory hyperalgesia. Importantly, several IFN-regulated genes (IRGs) were specific to nociceptor ion channels responsible for controlling neuronal activity and pain threshold. Therefore, STING promotes a pain-resolving IFN-I signaling pathway in nociceptors, thereby preventing sensitization and persistent pain

ORGANISM(S): Mus musculus

PROVIDER: GSE236865 | GEO | 2023/08/05

REPOSITORIES: GEO

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Induction of antiviral Interferon-Stimulated Genes (ISGs) by neuronal STING promotes the resolution of pain

Project description:Induction of antiviral Interferon-Stimulated Genes (ISGs) by neuronal STING promotes the resolution of pain

| PRJNA992544 | ENA

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