Interleukin-1β, Tumor Necrosis Factor-α, and Nitrite Levels in Febrile Seizures

Haspolat, Şenay; Mıhçı, Ercan; Çoşkun, Mesut; Gümüşlü, Saadet; Özbenm, Tomris; Yegin, Olcay

doi:10.1177/08830738020170101501

Cited by 111 publications

(96 citation statements)

References 16 publications

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“…IL-1β and IL-1R1 are up-regulated as a result of seizures in a variety of experimental models, including those induced by electrical stimulation, kainate, bicuculline, and hyperthermia [23,[25][26][27]. Elevated IL-1β and IL-1R1 have also been observed in brain tissue from patients with temporal lobe epilepsy and hippocampal sclerosis, and elevated IL-1β has been reported in cerebrospinal fluid (CSF) from children with febrile seizures [28,29]. In addition to increased IL-1 expression in patients with temporal lobe epilepsy, increases in IL-1β and inflammasome components have also been observed in other seizure disorders such as Rasmussen's encephalitis [30] and malformations of cortical development [31].…”

Section: Il-1β and Hmgb1 Expression In Seizuresmentioning

confidence: 98%

Epilepsy and the inflammasome: Targeting inflammation as a novel therapeutic strategy for seizure disorders

Edye¹,

Walker²,

Sills³

et al. 2014

Inflammasome

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Epilepsy is the most common serious brain disorder worldwide. Recent evidence from experimental models of epilepsy and clinical brain tissue from epilepsy surgery suggests inflammation may play a pathological role in this disorder. Activation of a multimolecular protein complex termed the ‘inflammasome’ occurs during inflammation to drive the innate immune response. Inflammasome activation, with release of inflammatory mediators including interleukin-1β and high-mobility group box-1, may play a crucial role in the development of epilepsy (epileptogenesis) after brain insult. Immunomodulatory drugs targeting the inflammasome pathway may represent a novel antiepileptogenic treatment strategy for epilepsy. This review summarises the current literature surrounding inflammasome activation and epilepsy.

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Section: Il-1β and Hmgb1 Expression In Seizuresmentioning

confidence: 98%

Epilepsy and the inflammasome: Targeting inflammation as a novel therapeutic strategy for seizure disorders

Edye¹,

Walker²,

Sills³

et al. 2014

Inflammasome

View full text Add to dashboard Cite

show abstract

“…Febrile seizures have been shown to be associated with increased IL-1β levels in CNS and blood plasma (68,69), and such IL-1β levels associated with a genetic polymorphism (70,71). IL-1β can act on the interleukin receptors on astrocytes and via the transcription factor NFκB induce a variety of molecules including the chemokines, cytokines and ERM proteins that are up-regulated in the sclerotic hippocampus.…”

Section: An Integrating Hypothesismentioning

confidence: 99%

Gene Expression in Temporal Lobe Epilepsy is Consistent with Increased Release of Glutamate by Astrocytes

Lee

Mane

Eid

et al. 2007

Mol Med

117

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Patients with temporal lobe epilepsy (TLE) often have a shrunken hippocampus that is known to be the location in which seizures originate. The role of the sclerotic hippocampus in the causation and maintenance of seizures in temporal lobe epilepsy (TLE) has remained incompletely understood despite extensive neuropathological investigations of this substrate. To gain new insights and develop new testable hypotheses on the role of sclerosis in the pathophysiology of TLE, the differential gene expression profile was studied. To this end, DNA microarray analysis was used to compare gene expression profiles in sclerotic and nonsclerotic hippocampi surgically removed from TLE patients. Sclerotic hippocampi had transcriptional signatures that were different from non-sclerotic hippocampi. The differentially expressed gene set in sclerotic hippocampi revealed changes in several molecular signaling pathways, which included the increased expression of genes associated with astrocyte structure (glial fibrillary acidic protein, ezrin-moesin-radixin, palladin), calcium regulation (S100 calcium binding protein beta, chemokine (C-X-C motif) receptor 4) and blood-brain barrier function (Aquaaporin 4, Chemokine (C-C-motif) ligand 2, Chemokine (C-C-motif) ligand 3, Plectin 1, intermediate filament binding protein 55kDa) and inflammatory responses. Immunohistochemical localization studies show that there is altered distribution of the gene-associated proteins in astrocytes from sclerotic foci compared with nonsclerotic foci. It is hypothesized that the astrocytes in sclerotic tissue have activated molecular pathways that could lead to enhanced release of glutamate by these cells. Such glutamate release may excite surrounding neurons and elicit seizure activity.

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“…Recent studies suggested that immunological aspects might be responsible for certain types of primary or secondary forms of epilepsy (for review see [13]). The findings of increased levels of cytokines such as interleukin-6 (IL-6) [14], interleukin-1β (IL-1β) [15] and interleukin-1 receptor antagonist (IL-1ra) [16] in cerebrospinal fluid from patients with epilepsy and the aggravating effect of IL-1β, one of the most important pro-inflammatory cytokines, in experimental models of epilepsy [8,9], suggest that the study of inflammatory factors involved in the pathogenesis of epileptic disorders can bring new insights into the molecular mechanisms and etiology of epilepsy.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin‐1 system

Oprica

Eriksson

Schultzberg

2003

J Cellular Molecular Medi

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The evidence of inflammatory processes in the clinical manifestations and neuropathological sequelae of epilepsy have accumulated in the last decade. Administration of kainic acid, an analogue of the excitatory amino acid glutamate, induces a characteristic behavioural syndrome and a reproducible pattern of neurodegeneration in several brain areas, closely resembling human temporal lobe epilepsy. Results from studies using the kainic acid model indicate that manipulation of pro-and anti-inflammatory cytokines can modify the outcome with regard to the behavioural syndrome as well as the neuropathological consequences. Interleukin-1 is one of the most important cytokines and has several actions in the brain that are critical for the host defense against injury and infection, and it is involved in the initiation of early stages of inflammation. It is believed that interleukin-1 plays a pivotal role in the neuroinflammation associated with certain forms of neurodegeneration, including cerebral ischemia, trauma and excitotoxic brain injury. 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-1β in this model of epilepsy.

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Interleukin-1β, Tumor Necrosis Factor-α, and Nitrite Levels in Febrile Seizures

Cited by 111 publications

References 16 publications

Epilepsy and the inflammasome: Targeting inflammation as a novel therapeutic strategy for seizure disorders

Epilepsy and the inflammasome: Targeting inflammation as a novel therapeutic strategy for seizure disorders

Gene Expression in Temporal Lobe Epilepsy is Consistent with Increased Release of Glutamate by Astrocytes

Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin‐1 system

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