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Similarity of inflammatory response in epileptic seizures and sepsis: does the sensitivity to sepsis in epileptic patients increase?
© Üzüm et al.; licensee BioMed Central Ltd. 2014
Published: 3 December 2014
It is known that the systemic response during sepsis is caused by proinflammatory mediators such as interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFα). The inflammatory response in sepsis causes disorders in the brain in addition to multiorgan dysfunctions including the kidneys and liver . Inducible nitric oxide synthase (iNOS) is induced in hepatocytes by sepsis and mediates hepatic injury . Matrix metalloproteinases (MMPs) play an important role in the formation of sepsis and mediate inflammatory response and tissue damage . On the other hand, there are some cases in which systemic inflammatory response occurs without the presence of infection such as epilepsy. Cytokines are well-known inflammatory mediators in the brain, and they increase following seizures. We previously demonstrated that pentyleneterazol (PTZ)-induced generalized epileptic seizures significantly increased inflammatory markers (TNFα, IL-1β, IL-6) in the brain and S100B in serum . In this preliminary study, we aimed to investigate the MMP2, MMP9, NOS, and myeloperoxidase activity in the liver and kidney and levels of serum proinflammatory cytokines following PTZ-induced generalized clonic-tonic seizures.
Adult Sprague-Dawley rats were divided into two groups as Control and PTZ groups. The Control group was given saline and the PTZ group was given 80 mg/kg PTZ i.p. Two hours after seizures, the rats were decapitated and a cardiac blood sample was drawn, and liver and kidneys were removed. Proinflammatory markers (IL-1βN, TNF-α, IL-6) were investigated in serum by ELISA. eNOS, iNOS, MMP2, and MMP9 levels were analyzed immunohistochemically in the liver and kidney.
Proinflammatory cytokines in control versus experimental groups
0.117 ± 0.042
0.775 ± 0.064
0.062 ± 0.010
0.783 ± 0.044
0.160 ± 0.012
0.0654 ± 0.026
The first findings show that long-term generalized clonic-tonic seizures markedly increase markers that mediate inflammation (iNOS, especially MMP2, MMP9, MPO) in the liver and kidney such as sepsis. In addition, proinflammatory markers (TNFα, IL-1β, IL-6) were found significantly high in serum. Thus, it is concluded that it will be worthwhile to determine whether epileptic seizures cause sensitivity to sepsis.
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