Increasing evidence corroborates the fundamental role of
neuroinflammation in the development of
epilepsy. Proinflammatory
cytokines (PICs) are crucial contributors to the inflammatory reactions in the brain. It is evidenced that epileptic
seizures are associated with elevated levels of PICs, particularly interleukin-1β (IL-1β),
IL-6, and
tumor necrosis factor-α (TNF-α), which underscores the impact of
neuroinflammation and PICs on hyperexcitability of the brain and epileptogenesis. Since the pathophysiology of
epilepsy is unknown, determining the possible roles of PICs in epileptogenesis could facilitate unraveling the pathophysiology of
epilepsy. About one-third of epileptic patients are drug-resistant, and existing treatments only resolve symptoms and do not inhibit epileptogenesis; thus, treatment of
epilepsy is still challenging. Accordingly, understanding the function of PICs in
epilepsy could provide us with promising targets for the treatment of
epilepsy, especially drug-resistant type. In this review, we outline the role of
neuroinflammation and its primary mediators, including IL-1β, IL-1α,
IL-6,
IL-17,
IL-18, TNF-α, and
interferon-γ (IFN-γ) in the pathophysiology of
epilepsy. Furthermore, we discuss the potential therapeutic targeting of PICs and
cytokine receptors in the treatment of
epilepsy.