ArticleCell communication and signaling : CCS2024
NLRP3 exacerbates EAE severity through ROS-dependent NET formation in the mouse brain.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
- A 'Tangled Web' in the CNS: unraveling neutrophil extracellular traps in neurological disorders.Molecular neurodegeneration · 2026Review
- Inhibition of HSPA8 alleviates experimental autoimmune encephalomyelitis via dual modulation of NLRP3 inflammasome activation: suppressing both NF-κB-mediated priming and ASC-dependent assembly.Cell death discovery · 2026Article
- GPNMB modulates neutrophil extracellular trap formation: therapeutic implications for ischemic stroke.Journal of neuroinflammation · 2026Article
- Targeting amino acid metabolic pathways: a novel therapeutic strategy for hyperuricemia-associated complications.Amino acids · 2026Review
- Organelle stress in NLRP3 inflammasome: a central mediator of neurodegenerative diseases.Molecular neurodegeneration · 2026Review
- Neutrophil extracellular traps in asthma and chronic obstructive pulmonary disease: pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Neutrophil extracellular traps in pulmonary fibrosis: mechanisms, immunity and therapeutic targets.Frontiers in immunology · 2026Review
- Neutrophil Extracellular Traps (NETs) in health and disease.Molecular biomedicine · 2025Review
- Sex-dependent effects of peptidylarginine deiminases on neutrophil function and long-term outcomes after spinal cord injury.Experimental neurology · 2025Article
- NETosis in hypersensitivity disorders.Molecular biology reports · 2025Review
- Advancements in research on the thrombo-inflammation mechanisms mediated by factor XII in ischemic stroke.Journal of thrombosis and thrombolysis · 2025Review
- High Fat Low Carbohydrate Diet Is Linked to CNS Autoimmunity Protection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SiglecF Expressing Neutrophils Exacerbate Th17-Mediated Autoimmune Neuroinflammation.Immune network · 2025Article
- NLRP3 activation induces BBB disruption and neutrophil infiltration via CXCR2 signaling in the mouse brain.Journal of neuroinflammation · 2025Article
- NETosis in Autoimmunity: Cell-Mediated vs. Ab-Mediated.Iranian journal of public health · 2025Article
- Neutrophil extracellular traps induced by neoadjuvant chemotherapy of breast cancer promotes vascular endothelial damage.Breast cancer research : BCR · 2025Article
- NETs-CD44-IL-17A Feedback Loop Drives Th17-Mediated Inflammation in Behçet's Uveitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular Mechanisms of Neutrophil Extracellular Traps in Promoting Gastric Cancer Epithelial-Mesenchymal Transition Through SERPINE-1 Expression.Journal of biochemical and molecular toxicology · 2025Article
- Chemokines as therapeutic targets for multiple sclerosis: a spatial and chronological perspective.Frontiers in immunology · 2025Review
- The role of NLRP3 inflammasome in multiple sclerosis: pathogenesis and pharmacological application.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNeutrophil extracellular trap (NET) has been implicated in the pathology of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). However, the specific contributions of NLRP3, a NET-associated molecule, to EAE pathogenesis and its regulatory role in NET formation remain unknown.
methodsTo investigate the detrimental effect of NETs supported by NLRP3 in MS pathogenesis, we induced EAE in WT and NLRP3 KO mice and monitored the disease severity. At the peak of the disease, NET formation was assessed by flow cytometry, immunoblotting, and immunofluorescence staining. To further identify the propensity of infiltrated neutrophils, NET-related chemokine receptors, degranulation, ROS production, and PAD4 expression levels were evaluated by flow cytometry. In some experiments, mice were injected with DNase-1 to eliminate the formed NETs.
resultsOur data revealed that neutrophils significantly infiltrate the brain and spinal cord and form NETs during EAE pathogenesis. NLRP3 significantly elevates NET formation, primarily in the brain. NLRP3 also modulated the phenotypes of brain-infiltrated and circulating neutrophils, augmenting CXCR2 and CXCR4 expression, thereby potentially enhancing NET formation. NLRP3 facilitates NET formation in a ROS-dependent and PAD4-independent manner in brain-infiltrated neutrophils. Finally, NLRP3-supported NET formation exacerbates disease severity, triggering Th1 and Th17 cells recruitment.
conclusionsCollectively, our findings suggest that NLRP3-supported NETs may be an etiological factor in EAE pathogenesis, primarily in the brain. This study provides evidence that targeting NLRP3 could be a potential therapeutic strategy for MS, specifically by attenuating NET formation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.