ArticleJournal of neuroinflammation2025
NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain.
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Neuroimmune interactions: from molecular mechanisms to therapeutic targets.Molecular biomedicine · 2026Review
- NLRP3 Deficiency Enhances Neutrophil Motility and Phagocytic Function in the Inflamed Kidney.Immune network · 2026Article
- Review
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Statins promote muscle metabolic danger and NLRP3-mediated myopathy via lower protein-prenylation and YAP.Science advances · 2026Article
- Integrated Blood Inflammatory Ratios and Cerebrospinal Fluid Blood‒Brain Barrier Dysfunction Predict Relapse Risk in Neuromyelitis Optica Spectrum Disorder.Brain and behavior · 2026Article
- Tau Oligomers Induce Brain Endothelial Cell Hyperpermeability and Increase NLRP3 Inflammasome Signaling and MMP-9 Activity.Microcirculation (New York, N.Y. : 1994) · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
NLRP3 is an intracellular sensor molecule that affects neutrophil functionality and infiltration in brain disorders such as experimental autoimmune encephalomyelitis (EAE). However, the detailed molecular mechanisms underlying the role of NLRP3 in these processes remain unknown. We found that NLRP3 is crucial for neutrophil infiltration, whereas dispensable for neutrophil priming. Notably, NLRP3 activation in neutrophils induced blood-brain barrier (BBB) disruption and neutrophil infiltration into the brain via CXCL1/2 secretion and subsequent activation of the CXCL1/2-CXCR2 signaling axis. Moreover, CXCL1 and CXCL2 in the inflamed brain directly reduced Claudin-5 expression, which regulates BBB permeability in brain endothelial cells. Furthermore, neutrophil-specific NLRP3 activation aggravated EAE pathogenesis by promoting CXCR2-mediated infiltration of both neutrophils and CD4
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Registered trials
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