Microglia mediate many important functions within the central nervous system, including maintaining homeostasis, acting as immune cells, and monitoring synapses. Under pathological conditions, changes in the morphological and functional characteristics of microglia occur. In the epileptic brain, this leads to dynamic changes in the microglial cell profile and different roles in epileptogenesis. Microglia play a crucial role in the formation of a pro-inflammatory microenvironment in the epileptic brain, thereby contributing to epileptogenesis. The inflammatory milieu in the brain, resulting from seizures, promotes neuronal hyperexcitability and leads to the occurrence of repeated epileptic seizures. A seizure followed by the production of pro-inflammatory mediators, which cause new seizures, collectively forms a positive feedback mechanism that promotes epileptogenesis. On the other hand, microglia can mediate a neuroprotective effect, such as suppressing inflammation, promoting the deposition of extracellular matrix, positively influencing white matter integrity, enhancing neuronal survival, and remodeling synapses. The amount of inflammatory mediators, the temporal exposure of brain parenchyma to their action, and the 24 balance between pro-inflammatory and anti-inflammatory or neuroprotective factors determine whether the outcome will be beneficial or harmful. The inflammatory component of epileptogenesis raises the question of new therapeutic possibilities based on the modulation of the inflammatory response in the brain, which would suppress harmful effects by targeting the pro-inflammatory mechanisms that exacerbate epilepsy.