ArticleClinical & translational immunology2021
Hypothesis: Febrile infection-related epilepsy syndrome is a microglial NLRP3 inflammasome/IL-1 axis-driven autoinflammatory syndrome.
Article in Clinical & translational immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Modulation of Gut Microbiome and Metabolome as One of the Potential Mechanisms of Ketogenic Diet Effect in the Treatment of Epilepsy.Nutrients · 2025Review
- De novo pathogenic CSF1R variant implicates microglial dysfunction in pathogenesis of febrile infection-related epilepsy syndrome.Epilepsia · 2025Article
- Minocycline in chronic management of febrile infection-related epilepsy syndrome (FIRES): a case series and literature review of treatment strategies.Acta epileptologica · 2025Review
- Potential inflammatory mechanisms of the ketogenic diet against febrile infection-related epilepsy syndrome.Acta epileptologica · 2025Review
- NLRP3 Inflammasome Inhibitors for Antiepileptogenic Drug Discovery and Development.International journal of molecular sciences · 2024Review
- The Role of Histone Deacetylases in NLRP3 Inflammasomesmediated Epilepsy.Current molecular medicine · 2024Review
- Connections Between Febrile Infection-Related Epilepsy Syndrome and Autoimmune Encephalitis. A Case Report of a Child With New Anti-neuronal Antibodies.Frontiers in pediatrics · 2022Article
- Central nervous system manifestations of monogenic autoinflammatory disorders and the neurotropic features of SARS-CoV-2: Drawing the parallels.Frontiers in pediatrics · 2022Review
Corrections and comments
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Authors and funding
2 authors.
Funding
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Abstract
FIRES (febrile infection-related epilepsy syndrome) is a protracted neuroinflammatory condition of obscure cause. It mainly afflicts school-age children and often leads to permanent neurological sequelae. Most treatments to date have been of limited efficacy, while ketogenic diet and anti-interleukin-1 therapy appear beneficial for some patients. Research into this clinical entity is hampered by its rarity and complexity. Nonetheless, accumulating evidence derived from basic investigations and clinical observations converges to implicate the autoinflammatory nature of this syndrome. A closer analysis of current literature suggests that microglia and the NLRP3 inflammasome might be the pivotal cellular and molecular players in FIRES pathogenesis, respectively. Through evidence synthesis, herein we formulate the working hypothesis of overactivation of microglial NLRP3 inflammasome/interleukin-1 axis as the driving event in FIRES by creating a proinflammatory and proconvulsive milieu. The reverberation between neuroinflammation and seizure forms a vicious cycle. The unique properties of microglia might also contribute to unopposed IL-1 signalling and incessant sterile neuroinflammation in this context. The potential therapeutic relevance of the proposed conceptual framework is discussed.
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