Also observed, T allele of IL-1β-31 and IL1-RAI/I were substantially positively correlated with drug resistance against those who responded well to antiepileptic drugs (AEDs).<b>Conclusions:</b> The significant association with IL-1β-31T and IL1-RAN*I alleles potentiated their useful role as predictive markers for the development of epilepsy and response to medical therapy.
Collectively, TRPV1 promoted astrocyte migration thus helped the infiltration of pro-inflammatory cytokines (TNF, IL-1β, IL-6, and iNOS) from astrocytes into the vicinity of neurons to promote epilepsy.
Furthermore, three modules were identified by protein-protein interaction analysis, and the potential hub genes, chemokine (C-C motif) ligand 3 and 4, chemokine (C-X-C motif) ligand 9, tumor necrosis factor-α and interleukin-1β, which are known to be closely associated with epilepsy, were identified.
Together, these findings suggest that patients with epilepsy responsive to immune modulation may have distinct autoinflammatory features supporting IL-1 blockade.
MMP3 can be induced by the pro-inflammatory cytokine IL-1β and is regulated by miR-155, suggesting a possible strategy to prevent epilepsy via reduction of inflammation.
The aim of the present study was to evaluate the expression of microRNA (miRNA)‑146a, phosphorylated (p)‑P65/P65, B‑cell lymphoma‑2(Bcl‑2)/Bcl‑2‑associated X protein (Bax) and pro‑inflammatory cytokines, such as interleukin (IL)‑6, IL‑1β and tumor necrosis factor (TNF‑α) in the brain tissue of rats with epilepsy.
These findings signified that IL-1 might inhibit the efficacy of low-frequency ES for epilepsy via the RhoA/ROCK signaling pathway, which may provide a theoretical basis for clinical treatment of epilepsy.
Together, we demonstrated that CCL2-CCR2 signaling contributes to neurodegeneration via STAT3 activation and IL-1β production after status epilepticus, providing potential therapeutic targets for the treatment of epilepsy.<b>SIGNIFICANCE STATEMENT</b> Epilepsy is a global concern and epileptic seizures occur in many neurological conditions.
This study evaluated the efficacy of gastrodin in combination with folate (FOL) and vitamin-B12 (V-B12) on patients with epilepsy after stroke (EAS) and its effect on high-mobility group protein B1 (HMGB-1), interleukin-1 (IL-1), and IL-6 serum levels.
Thus, this work identifies a pathogenic role of postnatal IL-1β/IL-1R1 pathway and subsequent prolonged prominent increase of endocannabinoid signaling in adult seizure susceptibility following prolonged FS, and highlights IL-1R1 as a potential therapeutic target for preventing the development of epilepsy after infantile FS.
The present meta-analysis showed that two alleles of proinflammatory cytokines (IL-1α-889 and IL-1β-511) in addition to the serum concentration of IL-6 were significantly associated with FS and epilepsy or both in various subgroup analyses.
For IL-1β, the most common genotype among the epilepsy group was the CT genotype with a 62% frequency; the T allele was the most common allele with a frequency of 34%.
To understand the role of genes encoding pro-inflammatory cytokines in epilepsy, this study aimed to evaluate the polymorphisms of the promoter regions of IL-1β-511C>T (rs16944), TNF-α-308G>A (rs1800629) and IL-6-174G>C (rs1800795) genes and to look into the interaction between these genes in influencing seizure susceptibility, seizure frequency and response to therapy.
More research is needed to fully establish the role of IL-1 in seizure generation and epilepsy, and to explore possible new treatment strategies that are based on interference with intracellular signaling cascades that are initiated when IL-1 binds to its receptor.
We immunocytochemically investigated the brain expression and cellular distribution pattern of IL-1beta, IL-1 receptor (IL-1R) types I and II and IL-1R antagonist (IL-1Ra) in FCD and GNT specimens, and we correlate these parameters with the clinical history of epilepsy in patients with medically intractable seizures.
In this review, we have summarized the experimental data available with regard to the involvement of the interleukin-1 system in kainic acid-induced changes in the brain and emphasized the modulatory role of interleukin-1beta in this model of epilepsy