{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T11:29:10Z","timestamp":1787138950916,"version":"build-2736575974"},"reference-count":414,"publisher":"MDPI AG","issue":"16","license":[{"start":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T00:00:00Z","timestamp":1787097600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Institute of Health, National Institute of Neurological Disorders and Stroke","award":["R01NS128421"],"award-info":[{"award-number":["R01NS128421"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Cells"],"abstract":"<jats:p>Background: Microbiome-based mechanisms have emerged as a key area of investigation in epilepsy, given the growing recognition that gut microbial communities can modulate central nervous system (CNS) function through the gut\u2013brain axis. Epilepsy is a common chronic neurological disorder affecting more than 65 million people worldwide, and despite the availability of anti-seizure medications (ASMs), approximately 30% of patients develop drug-resistant epilepsy. Current ASMs primarily suppress seizures rather than prevent disease progression, highlighting the need for alternative therapeutic strategies. In this context, increasing evidence supports a role for microbiota-dependent pathways in modulating seizure activity and treatment responsiveness. However, the mechanistic basis of these interactions remains incompletely understood. Methods: This narrative review synthesizes findings from the existing literature to examine the role of microbiota-derived metabolites, including neurotransmitters, vitamins, and the polyphenol metabolite S-equol, in gut\u2013brain communication relevant to epilepsy. Evidence was drawn from both preclinical animal models and clinical studies to provide an integrated, mechanistic perspective on how these pathways may influence central nervous system function and seizure susceptibility. Emphasis was placed on studies describing molecular, metabolic, and signaling mechanisms linking the gut microbiome to epileptogenesis and treatment response. Results: Current evidence indicates that communication between the gut and CNS occurs through neural pathways, such as the vagus nerve, as well as through circulating microbial metabolites. These metabolites can cross the intestinal barrier and, in some cases, the blood\u2013brain barrier (BBB), serving as key mediators of host\u2013microbiota signaling. Emerging studies suggest that while some microbial metabolites may directly influence neuronal hyperexcitability and seizure susceptibility, others likely exert secondary or modulatory effects through broader metabolic and immune pathways. However, the precise mechanisms underlying these interactions remain incompletely understood. Conclusions: Some microbial-derived metabolites may serve as promising biomarkers and mechanistic mediators of epilepsy; however, further investigation is needed to define the molecular and cellular pathways through which these metabolites influence seizure susceptibility and epileptogenesis.<\/jats:p>","DOI":"10.3390\/cells15161492","type":"journal-article","created":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T11:04:12Z","timestamp":1787137452000},"page":"1492","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Metabolic Outputs of the Gut Microbiome: Implications for Epilepsy"],"prefix":"10.3390","volume":"15","author":[{"given":"Allison","family":"Gallucci","sequence":"first","affiliation":[{"name":"Graduate Program in Translational Biology Medicine and Health, Virginia Tech, Roanoke, VA 24016, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3054-950X","authenticated-orcid":false,"given":"Xi","family":"Guo","sequence":"additional","affiliation":[{"name":"Cell, Development and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Devika","family":"Shukla","sequence":"additional","affiliation":[{"name":"Neuroscience Graduate Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7775-8600","authenticated-orcid":false,"given":"Susan L.","family":"Campbell","sequence":"additional","affiliation":[{"name":"Cell, Development and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2026,8,19]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"883","DOI":"10.1111\/j.1528-1167.2009.02481.x","article-title":"Estimation of the burden of active and life-time epilepsy: A meta-analytic approach","volume":"51","author":"Ngugi","year":"2010","journal-title":"Epilepsia"},{"key":"ref_2","doi-asserted-by":"crossref","first-page":"194","DOI":"10.1016\/j.seizure.2016.09.008","article-title":"Why epilepsy challenges social life","volume":"44","author":"Steiger","year":"2017","journal-title":"Seizure"},{"key":"ref_3","doi-asserted-by":"crossref","first-page":"a022426","DOI":"10.1101\/cshperspect.a022426","article-title":"Seizures and epilepsy: An overview for neuroscientists","volume":"5","author":"Stafstrom","year":"2015","journal-title":"Cold Spring Harb. 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