The brain-gut axis is a critical link between the brain and the gut, influencing various neurological and gastrointestinal disorders. This article explores the relationship between gut microbiota and epilepsy, highlighting the potential of microbiota-targeted interventions in managing the condition. Epilepsy, a neurological disorder characterized by unprovoked seizures, affects approximately 50 million people globally. Recent studies suggest that interventions such as fecal microbiota transplantation, probiotics, and the ketogenic diet (KD) can benefit drug-resistant epilepsy by modulating gut microbiota. However, the full extent of microbiota's role in epilepsy remains unclear, and more research is needed. The gut microbiota influences brain-gut interactions through nerve, endocrine, immune, and metabolic pathways. Dysbiosis in the gut microbiota has been linked to epilepsy, with studies showing differences in microbial composition between epilepsy patients and healthy individuals. For example, patients with drug-resistant epilepsy exhibited altered gut microbiota, including increased rare bacteria and changes in phylum abundance. These findings suggest that gut microbiota may play a significant role in epilepsy pathogenesis. The gut microbiota also influences the brain through the vagus nerve and endocrine pathways. Vagus nerve stimulation (VNS) is a therapy used for epilepsy, and gut microbiota can modulate neurotransmitter levels, such as 5-hydroxytryptamine (5-HT), which is involved in brain-gut communication. Additionally, gut microbiota can produce metabolites like short-chain fatty acids (SCFAs), which have anti-inflammatory and neuroprotective effects. SCFAs such as butyrate have been shown to reduce seizure intensity and increase seizure threshold. The gut microbiota also plays a role in the immune system, influencing the development and function of immune cells such as microglia and T cells. Imbalances in gut microbiota can lead to immune dysregulation, contributing to neuroinflammation and epilepsy. For example, Th1 cells, which secrete pro-inflammatory cytokines, can infiltrate the brain and promote neuroinflammation. Conversely, regulatory T cells (Treg cells) help maintain immune homeostasis and prevent excessive immune responses. Infections during pregnancy and early life have been linked to an increased risk of epilepsy, highlighting the importance of the immune system in epilepsy development. Animal studies further support the role of immunoinflammatory pathways in epilepsy, with factors such as TNF-α and MCP-1 playing a role in seizure susceptibility. Overall, the gut microbiota plays a complex and multifaceted role in epilepsy, influencing brain-gut interactions through various pathways. Targeting the gut microbiota through interventions such as fecal microbiota transplantation, probiotics, and the ketogenic diet may offer new therapeutic strategies for managing epilepsy. Further research is needed to fully understand the mechanisms and potential applications of microbiota-targeted therapies in epilepsy treatment.The brain-gut axis is a critical link between the brain and the gut, influencing various neurological and gastrointestinal disorders. This article explores the relationship between gut microbiota and epilepsy, highlighting the potential of microbiota-targeted interventions in managing the condition. Epilepsy, a neurological disorder characterized by unprovoked seizures, affects approximately 50 million people globally. Recent studies suggest that interventions such as fecal microbiota transplantation, probiotics, and the ketogenic diet (KD) can benefit drug-resistant epilepsy by modulating gut microbiota. However, the full extent of microbiota's role in epilepsy remains unclear, and more research is needed. The gut microbiota influences brain-gut interactions through nerve, endocrine, immune, and metabolic pathways. Dysbiosis in the gut microbiota has been linked to epilepsy, with studies showing differences in microbial composition between epilepsy patients and healthy individuals. For example, patients with drug-resistant epilepsy exhibited altered gut microbiota, including increased rare bacteria and changes in phylum abundance. These findings suggest that gut microbiota may play a significant role in epilepsy pathogenesis. The gut microbiota also influences the brain through the vagus nerve and endocrine pathways. Vagus nerve stimulation (VNS) is a therapy used for epilepsy, and gut microbiota can modulate neurotransmitter levels, such as 5-hydroxytryptamine (5-HT), which is involved in brain-gut communication. Additionally, gut microbiota can produce metabolites like short-chain fatty acids (SCFAs), which have anti-inflammatory and neuroprotective effects. SCFAs such as butyrate have been shown to reduce seizure intensity and increase seizure threshold. The gut microbiota also plays a role in the immune system, influencing the development and function of immune cells such as microglia and T cells. Imbalances in gut microbiota can lead to immune dysregulation, contributing to neuroinflammation and epilepsy. For example, Th1 cells, which secrete pro-inflammatory cytokines, can infiltrate the brain and promote neuroinflammation. Conversely, regulatory T cells (Treg cells) help maintain immune homeostasis and prevent excessive immune responses. Infections during pregnancy and early life have been linked to an increased risk of epilepsy, highlighting the importance of the immune system in epilepsy development. Animal studies further support the role of immunoinflammatory pathways in epilepsy, with factors such as TNF-α and MCP-1 playing a role in seizure susceptibility. Overall, the gut microbiota plays a complex and multifaceted role in epilepsy, influencing brain-gut interactions through various pathways. Targeting the gut microbiota through interventions such as fecal microbiota transplantation, probiotics, and the ketogenic diet may offer new therapeutic strategies for managing epilepsy. Further research is needed to fully understand the mechanisms and potential applications of microbiota-targeted therapies in epilepsy treatment.