ArticleMolecular brain2024
Systemic inflammation attenuates the repair of damaged brains through reduced phagocytic activity of monocytes infiltrating the brain.
Article in Molecular brain, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Etiological and immunological aspects of equine hoof canker.Veterinary research communications · 2026Article
- Hematopoietic Growth Factors Induce More Extensive Transcriptomic Remodeling in Cerebral Monocytes/Macrophages than in Microglia During the Chronic Phase of Traumatic Brain Injury.Molecular neurobiology · 2026Article
- Dysregulated Neuroimmune and Anhedonia-Like Behavioral Response Following Peripheral Immune Challenge in Mice Carrying the Val66Met Brain-Derived Neurotrophic Factor Polymorphism.Psychiatry international · 2025Article
- Systemic Inflammation Decreases Initial Brain Injury but Attenuates Neurite Extension and Synapse Formation during the Repair of Injured Brains.Experimental neurobiology · 2024Article
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Authors and funding
8 authors.
Funding
Abstract
In this study, we examined how systemic inflammation affects repair of brain injury. To this end, we created a brain-injury model by stereotaxic injection of ATP, a damage-associated molecular pattern component, into the striatum of mice. Systemic inflammation was induced by intraperitoneal injection of lipopolysaccharide (LPS-ip). An analysis of magnetic resonance images showed that LPS-ip reduced the initial brain injury but slowed injury repair. An immunostaining analysis using the neuronal marker, NeuN, showed that LPS-ip delayed removal of dead/dying neurons, despite the fact that LPS-ip enhanced infiltration of monocytes, which serve to phagocytize dead cells/debris. Notably, infiltrating monocytes showed a widely scattered distribution. Bulk RNAseq analyses showed that LPS-ip decreased expression of genes associated with phagocytosis, with PCR and immunostaining of injured brains confirming reduced levels of Cd68 and Clec7a, markers of phagocytic activity, in monocytes. Collectively, these results suggest that systemic inflammation affects properties of blood monocytes as well as brain cells, resulting in delay in clearing damaged cells and activating repair processes.
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