Interleukin-33 and oxidative stress in epilepsy patients

İnflammation and oxidative stress plays an important role in the etiology of epilepsy. Interleukin-33 (IL-33), a new member of the cytokine family associated with interleukin-1 (IL-1), has been found to play a role in pathogenesis of central nervous system diseases and cause the production of proinflammatory cytokines and oxidative stress molecules. Our aim was to investigate IL-33 and oxidative stress values (total antioxidant capacity (TAS), total oxidant capacity (TOS), and oxidative stress index (OSI)) in patients with epilepsy and to evaluate their relationship with each other.

The study included 60 patients with epilepsy and 35 healthy controls. The group of patients with epilepsy consisted of 21 patients with treatment-resistant epilepsy and 39 patients with well-controlled epilepsy. The patients with epilepsy were also classified as monotherapy and polytherapy group according to the number of antiepileptic drugs they used, and focal and generalized epilepsy group according to the seizure type. Serum IL-33, TAS, TOS and OSI levels were measured in the patients with epilepsy and the control group.

The mean serum TAS level was significantly lower in the all patients with epilepsy group compared to the control group, and the mean serum IL-33, TOS, and OSI levels were significantly higher. The mean serum TOS and OSI levels were significantly lower and TAS levels were significantly higher in the patients with well-controlled epilepsy than the patients with treatment-resistant epilepsy. While there was a positive correlation between serum IL-33 and OSI levels in the all patients with epilepsy group, a negative correlation was shown between IL-33 and TAS levels.

The IL-33/ST2 pathway may represent a new promising therapeutic strategy both for the treatment and the prevention of the disease.