ArticleAnnals of clinical and translational neurology2023
Drug-resistant seizures associated with hyperinflammatory monocytes in FIRES.
Article in Annals of clinical and translational neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 21 citations in OpenAlex.
- Chemokine Networks in Blood-Brain Barrier Regulation: Bidirectional Mechanisms, Clinical Translation, and Precision Therapeutic Prospects.Biomolecules · 2026Review
- Metabolomic identification and analysis of potential biomarkers of febrile seizures.BMC pediatrics · 2026Article
- Adaptive immune dysregulation drives new-onset refractory status epilepticus.Frontiers in immunology · 2026Review
- STAT3 signaling is associated with neuroimmune dysregulation in a Dravet syndrome model and pediatric drug-resistant epilepsy.Frontiers in neuroscience · 2026Article
- Standard complete blood count to predict long-term outcomes in febrile infection-related epilepsy syndrome (FIRES): A multicenter study.Epilepsia · 2025Article
- Cytokine, Chemokine, and Neurofilament Light Chain Signatures in LGI1 Autoimmune Encephalitis.Annals of clinical and translational neurology · 2025Article
- De novo pathogenic CSF1R variant implicates microglial dysfunction in pathogenesis of febrile infection-related epilepsy syndrome.Epilepsia · 2025Article
- Bursts of brain erosion: seizures and age-dependent neurological vulnerability.Trends in molecular medicine · 2025Review
- Advancing FIRES Treatment: The Potential of Intrathecal Dexamethasone.Annals of the Child Neurology Society · 2025Article
- Screening, Analysis, and Validation of Endoplasmic Reticulum Stress-Related DEGs in Epilepsy.Cellular and molecular neurobiology · 2025Article
- Combined Systemic Immunotherapy and Intrathecal Dexamethasone in Febrile Infection Related Epilepsy Syndrome.Annals of clinical and translational neurology · 2025Article
- Potential inflammatory mechanisms of the ketogenic diet against febrile infection-related epilepsy syndrome.Acta epileptologica · 2025Review
- Clinical characteristics of 27 children with febrile infection-related epilepsy syndrome in a single center.Pediatric discovery · 2024Article
- Status epilepticus in the ICU.Intensive care medicine · 2024Review
- Microglia and infiltrating macrophages in ictogenesis and epileptogenesis.Frontiers in molecular neuroscience · 2024Review
- Investigation of Correlation between Resistance to Diazepam and Expression of Inflammatory Markers in The Peripheral Blood of Patients with Status Epilepticus.Acta medica academica · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveTherapeutic strategies for patients with febrile infection-related epilepsy syndrome (FIRES) are limited, ad hoc, and frequently ineffective. Based on evidence that inflammation drives pathogenesis in FIRES, we used ex vivo stimulation of peripheral blood mononuclear cells (PBMCs) to characterize the monocytic response profile before and after therapy in a child successfully treated with dexamethasone delivered intrathecally six times between hospital Day 23 and 40 at 0.25 mg/kg/dose.
methodsPBMCs were isolated from serial blood draws acquired during refractory status epilepticus (RSE) and following resolution associated with intrathecal dexamethasone therapy in a previously healthy 9-year-old male that presented with seizures following Streptococcal pharyngitis. Cells were stimulated with bacterial or viral ligands and cytokine release was measured and compared to responses in age-matched healthy control PBMCs. Levels of inflammatory factors in the blood and CSF were also measured and compared to pediatric healthy control ranges.
resultsDuring RSE, serum levels of IL6, CXCL8, HMGB1, S100A8/A9, and CRP were significantly elevated. IL6 was elevated in CSF. Ex vivo stimulation of PBMCs collected during RSE revealed hyperinflammatory release of IL6 and CXCL8 in response to bacterial stimulation. Following intrathecal dexamethasone, RSE resolved, inflammatory levels normalized in serum and CSF, and the PBMC hyperinflammatory response renormalized. SIGNIFICANCE: FIRES may be associated with a hyperinflammatory monocytic response to normally banal bacterial pathogens. This hyperinflammatory response may induce a profound neutrophil burden and the consequent release of factors that further exacerbate inflammation and drive neuroinflammation. Intrathecal dexamethasone may resolve RSE by resetting this inflammatory feedback loop.
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