ArticleNeural regeneration research2023
Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury.
Article in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Semaglutide exerts neuroprotective effects by blocking the interleukin-17/NOD-like receptor family pyrin domain containing 3-mediated neuroinflammation pathway after traumatic brain injury.Neural regeneration research · 2026Article
- Th17 cells and IL-17A in traumatic brain injury: mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Astrocyte-derived CCL5-mediated CCR5Science advances · 2025Article
- β2 integrin regulates neutrophil trans endothelial migration following traumatic brain injury.Cell communication and signaling : CCS · 2025Article
- Roles and therapeutic potential of different extracellular vesicle subtypes on traumatic brain injury.Cell communication and signaling : CCS · 2023Review
- Autoimmune Neuroinflammatory Diseases: Role of Interleukins.International journal of molecular sciences · 2023Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After brain injury, infiltration and abnormal activation of neutrophils damages brain tissue and worsens inflammation, but the mediators that connect activated neutrophils with neuroinflammation have not yet been fully clarified. To identify regulators of neutrophil-mediated neuroinflammation after traumatic brain injury, a mouse model of traumatic brain injury was established by controlled cortical impact. At 7 days post-injury (sub-acute phase), genome-wide transcriptomic data showed that interleukin 17A-associated signaling pathways were markedly upregulated, suggesting that interleukin 17A may be involved in neuroinflammation. Double immunofluorescence staining showed that interleukin 17A was largely secreted by neutrophils rather than by glial cells and neurons. Furthermore, nuclear factor-kappaB and Stat3, both of which are important effectors in interleukin 17A-mediated proinflammatory responses, were significantly activated. Collectively, our findings suggest that neutrophil-derived interleukin 17A participates in neutrophil-mediated neuroinflammation during the subacute phase of traumatic brain injury. Therefore, interleukin 17A may be a promising therapeutic target for traumatic brain injury.
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