The production of IL-6 in acute epileptic seizure: A video-EEG study

Alapirtti, Tiina; Lehtimäki, Kai; Nieminen, Riina; Mäkinen, Riikka; Raitanen, Jani; Moilanen, Eeva; Mäkinen, Jussi; Peltola, Jukka

doi:10.1016/j.jneuroim.2017.12.008

Cited by 53 publications

(62 citation statements)

References 15 publications

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“…Similar basal anti-inflammatory effect was observed before by antiepileptic drugs that inhibits neuronal sodium channels like vinpocetine, carbamazepine and lamotrigine 30,50 . This basal inhibition might be clinically relevant to the current PGB-indicated conditions where elevated basal levels of these cytokines were clinically observed [7][8][9][10][11][12][13][14][15][16][17] .…”

Section: Discussionmentioning

confidence: 76%

“…Furthermore, a large panel of chemokines were elevated in the plasma and in the cerebrospinal fluid (CSF) in patients with this condition 11 . Similarly, elevated levels of the proinflammatory cytokines IL-6, TNF-α, IL-1β and IL-2 have been reported in epilepsy [12][13][14][15][16] . In patients with generalized anxiety disorders, an elevated level of several proinflammatory cytokines, including IL-6, TNF-α, IL-1β and IL-2 have been reported 17 .…”

mentioning

confidence: 67%

“…Peripheral inflammation is observed in the primary PGB-indicated conditions which all share elevated levels of IL-6, TNF-α, IL-1β and IL-2 cytokines [7][8][9][10][11][12][13][14][15][16][17] . Mitogen (LPS or ConA)-induced models of inflammation has long been used to assess the effects of drugs on macrophages-and T-cells-mediated proinflammatory cytokines production 34 and were also used to study the inflammation in PGB-indicated conditions [21][22][23][24]26 .…”

Section: Discussionmentioning

confidence: 99%

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Pregabalin inhibits in vivo and in vitro cytokine secretion and attenuates spleen inflammation in Lipopolysaccharide/Concanavalin A -induced murine models of inflammation

Abu-rish

Mansour

et al. 2020

Sci Rep

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is observed in the principal PGB-indicated conditions which share the alteration in IL-6, TNF-α, IL-2 and IL-1β cytokines level. Yet, reports on PGB immunomodulatory and anti-inflammatory effects are a few and focused mainly on in vitro assays, local inflammatory changes within the nervous system, and attenuation of the secretion of only IL-1β and TNF-α cytokines 18-20. In addition, PGB effects on cytokines secretion in immune cells, such as isolated splenocytes and peritoneal macrophages (PMs), and its effect on lymphoid organs, were not examined before. Therefore, there is a need to perform a simultaneous assessment of the effect of PGB on the secretion of the cytokines that were commonly elevated in the aforementioned PGB-indicated conditions (IL-6, TNF-α, IL-1β and IL-2) and to expand the investigation to its effect on lymphoid organs and cytokine secretion in immune cells. As peripheral inflammation and elevated systemic cytokines levels were demonstrated in the above-mentioned PGB-indicated conditions, we investigated in this study the effect of PGB on murine models of peripheral inflammation. In this study, we used for the first time, LPS and ConA-induced murine models of inflammation to examine the effect of PGB on peripheral proinflammatory cytokine secretion (IL-6, TNF-α, IL-1β and IL-2) in vitro and in vivo in BALB/c mice. LPS-model of inflammation has been employed before to study neuroinflammatory conditions, seizure and anxiety disorders in mice 21-25 , while ConA was used to investigate T-cell function in patients with fibromyalgia 26. Additionally, in this study, the effect of PGB on mitogen-induced inflammatory changes in the spleen, as a lymphoid organ, was also examined for the first time. Regarding in vitro investigation, the lack of reports that examined the effect of PGB on the secretion of cytokines in immune cells prompted us to investigate such effects of PGB on basal and mitogen-induced proinflammatory cytokines secretion in splenocytes and peritoneal macrophages (PMs).

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Section: Discussionmentioning

confidence: 76%

mentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Pregabalin inhibits in vivo and in vitro cytokine secretion and attenuates spleen inflammation in Lipopolysaccharide/Concanavalin A -induced murine models of inflammation

Abu-rish

Mansour

et al. 2020

Sci Rep

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“…Experimental data from rodent models confirmed that enhanced activation of inflammatory pathways can contribute to enhanced excitability and lowered thresholds in the epileptic brain [3][4][5]. Moreover, increased expression rates of various pro-inflammatory mediators have been demonstrated in brain tissue from rodent epilepsy models as well as human patients with epilepsy [1,[6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 78%

Molecular alterations of the TLR4-signaling cascade in canine epilepsy

et al. 2020

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Background: Cumulating evidence from rodent models points to a pathophysiological role of inflammatory signaling in the epileptic brain with Toll-like receptor-4 signaling acting as one key factor. However, there is an apparent lack of information about expression alterations affecting this pathway in canine patients with epilepsy. Therefore, we have analyzed the expression pattern of Toll-like receptor 4 and its ligands in brain tissue of canine patients with structural or idiopathic epilepsy in comparison with tissue from laboratory dogs or from owner-kept dogs without neurological diseases. Results: The analysis revealed an overexpression of Toll-like receptor-4 in the CA3 region of dogs with structural epilepsy. Further analysis provided evidence for an upregulation of Toll-like receptor-4 ligands with high mobility group box-1 exhibiting increased expression levels in the CA1 region of dogs with idiopathic and structural epilepsy, and heat shock protein 70 exhibiting increased expression levels in the piriform lobe of dogs with idiopathic epilepsy. In further brain regions, receptor and ligand expression rates proved to be either in the control range or reduced below control levels. Conclusions: Our study reveals complex molecular alterations affecting the Toll-like receptor signaling cascade, which differ between epilepsy types and between brain regions. Taken together, the data indicate that multitargeting approaches modulating Toll-like receptor-4 signaling might be of interest for management of canine epilepsy. Further studies are recommended to explore respective molecular alterations in more detail in dogs with different etiologies and to confirm the role of the pro-inflammatory signaling cascade as a putative target.

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“…42 At 6 hours after focal unaware or secondary generalized tonicclonic seizures in patients with MTLE or extratemporal epilepsies, only the MTLE group showed a significant rise in plasma levels of IL6. 43 Saliva may represent a less invasive and less expensive method for quantification of this biomarker and further studies are needed to validate this finding.…”

Section: Discussionmentioning

confidence: 99%

Differential Activation of Neuroinflammatory Pathways in Children with Seizures: A Cross-Sectional Study

Bartolini

Moran

Norato

et al. 2019

Preprint

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Background: Experimental and clinical findings suggest a crucial role of inflammation in epileptogenesis. We aimed to analyze levels of inflammatory cytokines in plasma and saliva from children with acute seizures and healthy controls and measure their associations with HHV6 and EBV infection. Methods: We analyzed plasma from 36 children within 24 hours of acute seizures (cases) and 43 healthy controls and saliva from 44 cases and 44 controls with a multiplex immunoassay. Saliva from all controls and 65 cases and blood from 26 controls and 35 cases were also analyzed by ddPCR for viral DNA. Statistical analysis included Wilcoxon Rank Sum test, Fisher’s exact test, ANOVA and Spearman correlation. Results: Compared to controls, children with breakthrough seizures (n=18) had higher levels of CCL11 (p<0.001), CCL26 (p<0.001), IL-8 (p=0.03), CCL4 (p=0.02) in plasma. Children with new onset seizures (n=13) showed higher levels of CCL11 (p=0.05) and IL-6 (p=0.01). Patients with febrile seizures (n=5) had higher levels of IFNg (p<0.001), IL-6 (p<0.001), IL-10 (p<0.001), CXCL10 (p=0.001). CCL11 was higher with 3 or more seizures (p=0.01), seizures longer than 10 minutes (p=0.001) and when EEG showed focal slowing (p=0.02). In saliva, febrile seizures had higher levels of IL-1β (n=7, p=0.04) and new onset seizures had higher IL-6 (n=15, p=0.02). Plasma and saliva cytokine levels did not show correlation. Frequency of HHV-6 and EBV detection was similar across seizure types and not different than controls. We found no correlation between viral load and cytokine levels Conclusions: We showed differential activation of neuroinflammatory pathways in plasma from different seizure etiologies compared to controls, unrelated to HHV-6 infection.

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The production of IL-6 in acute epileptic seizure: A video-EEG study

Cited by 53 publications

References 15 publications

Pregabalin inhibits in vivo and in vitro cytokine secretion and attenuates spleen inflammation in Lipopolysaccharide/Concanavalin A -induced murine models of inflammation

Pregabalin inhibits in vivo and in vitro cytokine secretion and attenuates spleen inflammation in Lipopolysaccharide/Concanavalin A -induced murine models of inflammation

Molecular alterations of the TLR4-signaling cascade in canine epilepsy

Differential Activation of Neuroinflammatory Pathways in Children with Seizures: A Cross-Sectional Study

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