Single Nucleotide Polymorphism and Production of IL-1β and IL-10 Cytokines in Febrile Seizures

Abstract

Inflammation and genetics may play a role in the pathogenesis of febrile seizures. The aim of this study was to investigate the spontaneous and lipopolysaccharide (LPS)-induced production of IL-1β and IL-10, and the association between IL-1β (-511) and IL-10 (-1082) single nucleotide polymorphisms with LPS-induced cytokine production. The study included 92 febrile seizure patients and 132 healthy controls. First, we isolated genomic DNA and by using PCR-RFLP we genotyped the individuals for the cytokines gene polymorphism. Second, peripheral mononuclear cells of the individuals were isolated and stimulated with LPS to measure secretion capacity of IL-1β and IL-10 using specific ELISA kits. We found that both the IL-1β and IL-10 production was increased in febrile seizures. The rapid increase of IL-1β production in the supernatants of the LPS-induced cells was significantly higher at the fourth and the twenty-fourth hours in febrile and complex febrile seizures, respectively. The distribution of IL-10 (-1082) G allele differs significantly between cases and controls. The IL-1β (-511) G/A and the IL-10 (-1082) G/A genotype combination was found to be higher in patients with febrile seizure. Our results showed that IL-1β and IL-10 production was not influenced by the single nucleotide polymorphisms in the pathogenesis of febrile seizures.

Reduced cerebrospinal fluid levels of interleukin-10 in children with febrile seizures

“…It was generally reported that in FS patients, higher serum IL-10 levels [18,21,22], and higher IL-10 response in their peripheral blood mononuclear cells [3,23] were present. The higher IL-10 levels in serum have been thought to be associated with the defensive mechanism that emerges secondarily to the increase in proinflammatory cytokines [3,18,21].…”

Proinflammatory and anti-inflammatory cytokines in febrile seizures and epilepsy: systematic review and meta-analysis

“…With regard to the defined inclusion and exclusion criteria, a total of 25 case-control genetic association studies were included in the present analysis. Eventually, with regard to the number of studies (a minimum of three studies for each variant), we carried out meta-analyses for IL-1α-889 with four studies (Kanemoto et al, 2000;Peltola et al, 2001;Haspolat et al, 2005;Ozkara et al, 2006), IL-1β-511 with 20 studies (Heils et al, 2000;Buono et al, 2001;Peltola et al, 2001;Tilgen et al, 2002;Virta et al, 2002a;Chou et al, 2003c;Jin et al, 2003;Kanemoto et al, 2003;Cavalleri et al, 2005;Haspolat et al, 2005;Chung et al, 2006;Matsuo et al, 2006;Ozkara et al, 2006;Shu-hua et al, 2006;Yoon et al, 2008;Serdaroğlu et al, 2009;Chou et al, 2010;Kira et al, 2010;Nur et al, 2012a;Tiwari et al, 2012), IL-1Ra with six studies (Kanemoto et al, 2000;Tsai et al 2002a;Haspolat et al, 2005;Matsuo et al, 2006;Serdaroğlu et al, 2009;Chou et al, 2010), IL-6-572 with three studies (Ishizaki et al, 2009;Chou et al, 2010;Nur et al, 2012b), and TNF-α-308 with three studies (Chou et al, 2010;Khoshdel et al, 2012;Tiwari et al...…”

Association Analysis of Interleukin-1β, Interleukin-6, and HMGB1 Variants with Postictal Serum Cytokine Levels in Children with Febrile Seizure and Generalized Epilepsy with Febrile Seizure Plus

“…Therefore, genetic variants that up-regulate cytokine production can increase the degree of inflammatory responses to infection or other stimuli, which may subsequently predispose subjects to develop fever-provoked seizures. In vitro stimulation of peripheral blood mononuclear cells with lipopolysaccharide, mimicking bacterial infection, reportedly demonstrates that IL-1β production is higher in FS children than in controls 24…”