Systemic inflammatory response syndrome in the course of status epilepticus: 7-year, two-center observational study

Szklener, Sebastian; Korchut, Agnieszka; Godek, Magdalena; Balicka‐Adamik, Luiza; Bielecki, Dariusz; Ręjdak, Robert; Rejdak, Konrad

doi:10.1016/j.eplepsyres.2017.09.003

Cited by 19 publications

(15 citation statements)

References 8 publications

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“…In a comprehensive FIRES literature review, we found several patients with similar clinical deterioration and rash about 4 weeks after illness onset, 1,11,17,18 but none mentioned HLH screening. Although the cooccurrence of systemic inflammatory response syndrome has been reported after status epilepticus, 19 to our knowledge, the coexistence of FIRES and HLH has not been described previously. We summarize our hypothesized mechanisms for the association between FIRES and secondary HLH observed in our cohort (Figure 4) initiating with a nonspecific febrile illness triggering release of inflammatory molecules.…”

Section: Discussionmentioning

confidence: 68%

“…In a comprehensive FIRES literature review, we found several patients with similar clinical deterioration and rash about 4 weeks after illness onset, but none mentioned HLH screening. Although the co‐occurrence of systemic inflammatory response syndrome has been reported after status epilepticus, to our knowledge, the coexistence of FIRES and HLH has not been described previously.…”

Section: Discussionmentioning

confidence: 73%

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Fueling the FIRES: Hemophagocytic lymphohistiocytosis in febrile infection‐related epilepsy syndrome

et al. 2018

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Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 73%

Fueling the FIRES: Hemophagocytic lymphohistiocytosis in febrile infection‐related epilepsy syndrome

et al. 2018

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“…30,31 A strong relationship between neuroinflammation and SE has been reported in previous studies. 4,32 In both animal models and patients with SE, increasing evidence has shown that elevated inflammation in the brain during SE plays a decisive role in persistent seizures and long-term sequelae. 33 In vivo evidence has shown that the site of inflammation contains high concentrations (hundreds of micromoles) of extracellular ATP, highlighting the vital role of extracellular ATP in inflammation.…”

Section: Discussionmentioning

confidence: 99%

<p>Astaxanthin Attenuates Neuroinflammation in Status Epilepticus Rats by Regulating the ATP-P2X7R Signal</p>

Wang

Deng

Xie

et al. 2020

DDDT

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Background: As a life-threatening neurological emergency, status epilepticus (SE) is often refractory to available treatment. Current studies have shown a causal role of neuroinflammation in patients with lower seizure thresholds and driving seizures. The ATP-gated purinergic P2X7 receptor (P2X7R) is mainly expressed on the microglia, which function as gatekeepers of inflammation. Although emerging evidence has demonstrated significant anti-inflammatory effects of astaxanthin (AST) in SE, the associated mechanism remains unclear. Therefore, this study aimed to clarify the effects of AST on P2X7R-related inflammation in SE. Methods: SE was induced in rats using lithium-pilocarpine, and AST was administered 1 h after SE induction. Rat microglia were treated with lipopolysaccharide (LPS), AST, ATP, 2,3-O-4-benzoyl-4-benzoyl-ATP (BzATP) and oxidized ATP (oxATP). The Morris water maze, immunohistochemistry, and Nissl staining were performed in rats. Expressions of P2X7R and inflammatory cytokines (such as cycloxygenase-2 (Cox-2), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α)) were detected using real-time polymerase chain reaction (RT-PCR) and Western blot (WB) both in rats and microglia. ATP concentration in the microglia was evaluated using ELISA. Results: The AST alleviated hippocampal injury and improved cognitive dysfunction induced by SE. AST also effectively inhibited inflammation and downregulated P2X7R expression in both rat brain and microglia. The results also showed that AST reduced the extracellular ATP levels and that P2X7R expression could be increased by extracellular ATP. In addition, BzATP upregulates the expression of P2X7R and inflammatory factors in microglia. Conversely, it downregulates the expression of P2X7R and inflammatory factors. Conclusion: Our study suggests that AST attenuated ATP-P2X7R mediated inflammation in SE.

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“…Further functional prediction and lncRNA-miRNA-mRNA co-expression network analysis indicated that the up-regulated hub lncRNAs in turquoise module were involved in SE progression through regulation of apoptosis, Rap1 signalling pathway, cAMP signalling pathway, chemokine signalling pathway, inflammatory mediator regulation of TRP channels and PI3K-Akt signalling pathway, which have been demonstrated to play an important role in the pathogenesis of SE. [31][32][33][34][35] Furthermore, the in vitro model was studied to confirm the functional role of an identified hub lncRNA (NONRATT010788.2) that was associated with apoptosis. The constructed co-expression network indicated that lncRNA, NONRATT010788.2, inversely correlated with miR-324-3p, which plays a negative role in apoptosis.…”

Section: Knockdown Of Nonratt0107882 Inhibits Neuronal Apoptosismentioning

confidence: 99%

Expression and functional analysis of lncRNAs in the hippocampus of immature rats with status epilepticus

Gan

Huang

et al. 2019

J Cellular Molecular Medi

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Long non‐coding RNAs (lncRNAs) have been implicated in the regulation of gene expression at various levels. However, to date, the expression profile of lncRNAs in status epilepticus (SE) was unclear. In our study, the expression profile of lncRNAs was investigated by high‐throughput sequencing based on a lithium/pilocarpine‐induced SE model in immature rats. Furthermore, weighted correlation network analysis (WGCNA), gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed to construct co‐expression networks and establish functions of the identified hub lncRNAs in SE. The functional role of a hub lncRNA (NONRATT010788.2) in SE was investigated in an in vitro model. Our results indicated that 7082 lncRNAs (3522 up‐regulated and 3560 down‐regulated), which are involved in cell proliferation, inflammatory responses, angiogenesis and autophagy, were dysregulated in the hippocampus of immature rats with SE. Additionally, WGCNA identified 667 up‐regulated hub lncRNAs in turquoise module that were involved in apoptosis, inflammatory responses and angiogenesis via regulation of HIF‐1, p53 and chemokine signalling pathways and via inflammatory mediator regulation of TRP channels. Knockdown of an identified hub lncRNA (NONRATT010788.2) inhibited neuronal apoptosis in vitro. Taken together, our study is the first to demonstrate the expression profile and potential function of lncRNAs in the hippocampus of immature rats with SE. The defined hub lncRNAs may participate in the pathogenesis of SE via lncRNA‐miRNA‐mRNA network.

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Systemic inflammatory response syndrome in the course of status epilepticus: 7-year, two-center observational study

Cited by 19 publications

References 8 publications

Fueling the FIRES: Hemophagocytic lymphohistiocytosis in febrile infection‐related epilepsy syndrome

Fueling the FIRES: Hemophagocytic lymphohistiocytosis in febrile infection‐related epilepsy syndrome

<p>Astaxanthin Attenuates Neuroinflammation in Status Epilepticus Rats by Regulating the ATP-P2X7R Signal</p>

Expression and functional analysis of lncRNAs in the hippocampus of immature rats with status epilepticus

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