AI Article Synopsis
- Innate immune responses to RNA viruses, particularly West Nile virus, can lead to significant neurological issues, including memory disorders due to inflammation in the brain.
- During the infection, macrophages produce the cytokine IL-1β, but even after recovery, astrocytes continue to produce high levels of IL-1β, affecting the functioning of neural stem cells (NSC) in the hippocampus.
- This continuous IL-1 signaling results in abnormal production of astrocytes instead of neurons, hindering synapse repair and contributing to deficits in spatial learning abilities.
Article Abstract
Innate immune responses to emerging RNA viruses are increasingly recognized as having significant contributions to neurologic sequelae, especially memory disorders. Using a recovery model of West Nile virus (WNV) encephalitis, we show that, while macrophages deliver the antiviral and anti-neurogenic cytokine IL-1β during acute infection; viral recovery is associated with continued astrocyte inflammasome-mediated production of inflammatory levels of IL-1β, which is maintained by hippocampal astrogenesis via IL-1R1 signaling in neural stem cells (NSC). Accordingly, aberrant astrogenesis is prevented in the absence of IL-1 signaling in NSC, indicating that only newly generated astrocytes exert neurotoxic effects, preventing synapse repair and promoting spatial learning deficits. Ex vivo evaluation of IL-1β-treated adult hippocampal NSC revealed the upregulation of developmental differentiation pathways that derail adult neurogenesis in favor of astrogenesis, following viral infection. We conclude that NSC-specific IL-1 signaling within the hippocampus during viral encephalitis prevents synapse recovery and promotes spatial learning defects via altered fates of NSC progeny that maintain inflammation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10236567 | PMC |
| http://dx.doi.org/10.1016/j.bbi.2021.10.010 | DOI Listing |
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