Paediatric epilepsy is a multifaceted neurological disorder with various aetiologies. Up to 30% of patients are considered drug-resistant. The background impact of interfering inflammatory and neuronal pathways has been closely linked to paediatric epilepsy. The characteristics of the inflamed state have been described not only in epilepsies, which are considered prototypes of an inflammatory pathophysiology, but also in patients with drug-resistant epilepsy, especially in epileptic encephalopathies. The imbalance of different cytokine levels was confirmed in several epileptic models. Chemokines are new targets for exploring neuroimmune communication in epileptogenesis, which control leukocyte migration and have a possible role in neuromodulation. Additionally, prostaglandin E2 (PGE2) is an important effector molecule for central neural inflammatory responses and may influence drug responsiveness. We measured the serum interictal quantitative levels of chemokines (CCL2, CCL4, CCL11) and PGE2 in correlation with the seizure frequency and severity in controlled and intractable childhood epilepsies. Our refractory seizure group demonstrated significantly increased concentrations of eotaxin (CCL11) compared to the controlled epilepsy group. The higher level of CCL11 was correlated with an increased seizure frequency, while the PGE2 levels were associated with the severity of seizure and epilepsy, supporting the findings that proinflammatory cytokines may contribute to epileptogenesis and possibly have a role in developing seizure resistance.
Background: Epilepsy is the most frequent chronic neurologic disorder of childhood, with a reported higher incidence in underdeveloped countries. The pathogenesis of epilepsy involves complex mechanisms that are still not fully understood. In recent years, researchers have shown increasing interest in understanding the role of inflammation in epilepsy. One such component of the neuroinflammatory cascade is Interferon-Gamma (IFN-γ), a pro-inflammatory cytokine known for its role in immune responses. However, recent studies have revealed that IFN-γ possesses multifaceted properties, including potential neuroprotective and anticonvulsant effects. Multiple studies have reported elevated levels of IFN-γ in the serum, cerebrospinal fluid, and brain tissue of patients with epilepsy. The precise mechanisms through which IFNγ contributes to epilepsy remain incompletely understood. Objectives: The present study aimed to compare IFN-γ levels in drug-resistant epilepsy patients with those with well-controlled epilepsy and healthy controls. Methods: This prospective cross-sectional study enrolled 56 children: 20 with drug-resistant epilepsy, 20 with well-controlled epilepsy, and 16 healthy controls matched in demographic characteristics. Venous blood samples were collected from all participants for cytokine (chemokines, PGE2, and interferon-gamma (IFN-γ) analysis. Results: IFN-γ levels were not elevated in the study groups. The results indicate a considerable heterogeneity in IFN-γ levels among different types of epilepsy. The interquartile range (IQR) of targeted IFN-γ was lower in the drug-resistant epilepsy patients compared to well-controlled epilepsy and healthy control groups. Conclusions: The role of IFN-γ in epilepsies is complex and context-dependent. The precise role of IFN-γ in epilepsy warrants exploration; further research is needed to explore the current understanding of the relationship between IFN-γ and childhood epilepsy. The findings from this study may contribute to a better understanding of the role of cytokines in the pathogenesis of epilepsy and could potentially support the development of novel therapeutic approaches targeting cytokine dysregulation in epilepsy.
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