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Type I Interferon Response Is Mediated by NLRX1-cGAS-STING Signaling in Brain Injury.

Lauren E Fritsch1, Jing Ju2, Erwin Kristobal Gudenschwager Basso3

  • 1Translational Biology, Medicine, and Health Graduate Program, Virginia Polytechnic Institute and State University, Roanoke, VA, United States.

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Summary

The Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes (cGAS-STING) pathway drives inflammation and neuronal damage after traumatic brain injury (TBI). Inhibiting this pathway, possibly triggered by mitochondrial DNA, offers neuroprotection.

Keywords:
STINGbrain injurycGASinflammationinnate immunity

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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Inflammation significantly contributes to neuronal death and dysfunction post-traumatic brain injury (TBI).
  • Interferons are emerging as key regulators of the inflammatory response in TBI.
  • The Cyclic GMP-AMP Synthase-Stimulator of Interferon Genes (cGAS-STING) pathway's role in TBI is under investigation.

Purpose of the Study:

  • To evaluate the role of the cGAS-STING signaling pathway in a murine model of TBI.
  • To investigate the potential trigger of mitochondrial DNA in the cGAS-STING pathway activation.
  • To explore the regulatory role of NLR containing X1 (NLRX1) in the cGAS-STING pathway within the brain.

Main Methods:

  • Controlled cortical impact (CCI) or sham injury was performed on wildtype, cGAS knockout, STING knockout, and NLRX1 knockout mice.
  • Histopathological tissue damage was assessed using non-biased stereology.
  • mRNA and protein levels were analyzed using qPCR and western blot, respectively.

Main Results:

  • STING and Type I interferon-stimulated genes showed a bi-phasic upregulation post-CCI.
  • Loss of cGAS or STING conferred neuroprotection, with reduced inflammation at 24 hours post-injury.
  • Mitochondrial DNA was detected in the cytosol post-TBI, suggesting it as a potential cGAS-STING pathway trigger. NLRX1 was identified as an upstream regulator.

Conclusions:

  • The cGAS-STING-mediated Type I interferon signaling axis is critical for neural tissue damage following TBI.
  • Mitochondrial DNA is a potential trigger for this pathway in the context of TBI.
  • NLRX1 acts as an upstream regulator of the cGAS-STING pathway in the brain.