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: The clinical heterogeneity of autism spectrum disorders (ASDs) results from dynamic interactions between genetic susceptibility and environmental exposures. Autism is increasingly recognized as involving neuroimmune dysregulation, which may contribute to ASD severity. Several studies indicate that ASD patients exhibit increased levels of VCAM-1, suggesting endothelial dysfunction and enhanced leukocyte infiltration into the brain, which may have adverse bearing on synaptic plasticity, axon growth, and repulsion. Similarly, elevated PGE2 drives microglial activation and excitotoxicity. The present study examines possible links between VCAM-1 and PGE2 levels and ASD severity. Methods: VCAM-1 and PGE₂ concentrations were measured in children with ASD aged 2–6 years and analyzed for age effects and correlations with behavioral severity. Participants were grouped as mild, moderate, or severe based on Autism Diagnostic Observation Schedule-2 (ADOS-2) scores. Results: VCAM-1 levels were subnormal in 39.3% (n = 24), and PGE₂ levels were above normal in 32.8% (n = 20). Mean VCAM-1 levels decreased significantly with age (F(4, 56) =2.98, p = 0.026) and also, were higher in moderate (U = 36.00, Z = −3.96, p < 0.001) and severe (U = 155.50, Z =−2.70, p = 0.007) ASD groups, with mean ranks rising from 14.46 (mild) to 41.13 (severe). PGE₂ did not differ between severity and age groups (p > 0.05). VCAM-1 correlated moderately with ADOS-2 scores (rho = 0.577, p < 0.001), whereas PGE2 did not (rho = 0.108, p = 0.406), suggesting higher VCAM-1 is linked to increased behavioral severity in ASD. Conclusions: Inflammation-related biomarkers could be reflecting a heterogeneous set of neuroimmune mechanisms underlying ASD, which may drive behavioral outcomes.