The protective effects of interleukin-18 and interferon-γ on neuronal damages in the rat hippocampus following status epilepticus

Ryu, Hea Jin; Kim, J.-E.; Kim, M.-J.; Kwon, Hyung‐Joo; Suh, Sang Won; Song, Hong-Ki; Kang, Tae‐Cheon

doi:10.1016/j.neuroscience.2010.07.048

Cited by 36 publications

(23 citation statements)

References 52 publications

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“…For example, type 1 interferons have been regarded as anti-inflammatory within the brain due to their ability to limit leukocyte infiltration (Prinz et al, 2008) and reduce expression of pro-inflammatory cytokines including IL-1β and TNFα (Teige et al, 2006). IFNγ has also been shown to elicit antiinflammatory effects (Muhl and Pfeilschifter, 2003), protect neurons from damage initiated by viral infection (Geiger et al, 1997;Rodriguez et al, 2003), protect cultured hippocampal neurons against glutamate-induced excitotoxic death (Lee et al, 2006) and alleviate status epilepticus-induced neuronal damage in the hippocampus of rats (Ryu et al, 2010). Furthermore, enhancement of both type 1 and 2 interferons limits inflammation and disease progression in models of multiple sclerosis (Lin et al, 2007;Bowen and Olson, 2013;Naves et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

FAAH-mediated modulation of TLR3-induced neuroinflammation in the rat hippocampus

Henry

Kerr

Finn

et al. 2014

Journal of Neuroimmunology

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Section: Discussionmentioning

confidence: 99%

FAAH-mediated modulation of TLR3-induced neuroinflammation in the rat hippocampus

Henry

Kerr

Finn

et al. 2014

Journal of Neuroimmunology

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“…Indeed, the kynurenine pathway can be activated by the release of proinflammatory cytokines, which have been implicated in the pathophysiology of epilepsy, especially in the context of cortical dysplasia and glioneuronal tumors [41–43]. Several cytokines, including IFN-γ, are stimulated by seizures and serve as inducers of IDO [44, 45], and they may represent a potential pharmacological target for treatment of epileptogenic lesions.…”

Section: Discussionmentioning

confidence: 99%

Increased tryptophan transport in epileptogenic dysembryoplastic neuroepithelial tumors

et al. 2011

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Dysembryoplastic neuroepithelial tumors (DNTs) are typically hypometabolic but can show increased amino acid uptake on positron emission tomography (PET). To better understand mechanisms of amino acid accumulation in epileptogenic DNTs, we combined quantitative α-[11C]methyl-L-tryptophan (AMT) PET with tumor immunohistochemistry. Standardized uptake values (SUVs) of AMT and glucose were measured in 11 children with temporal lobe DNT. Additional quantification for AMT transport and metabolism was performed in 9 DNTs. Tumor specimens were immunostained for the L-type amino acid transporter 1 (LAT1) and indoleamine 2,3-dioxygenase (IDO), a key enzyme of the immunomodulatory kynurenine pathway. All 11 tumors showed glucose hypometabolism, while mean AMT SUVs were higher than normal cortex in eight DNTs. Further quantification showed increased AMT transport in seven and high AMT metabolic rates in three DNTs. Two patients showing extratumoral cortical increases of AMT SUV had persistent seizures despite complete tumor resection. Resected DNTs showed moderate to strong LAT1 and mild to moderate IDO immunoreactivity, with the strongest expression in tumor vessels. These results indicate that accumulation of tryptophan in DNTs is driven by high amino acid transport, mediated by LAT1, which can provide the substrate for tumoral tryptophan metabolism through the kynurenine pathway, that can produce epileptogenic metabolites. Increased AMT uptake can extend to extratumoral cortex, and presence of such cortical regions may increase the likelihood of recurrent seizures following surgical excision of DNTs.

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“…The pump was placed in a subcutaneous pocket in the dorsal region. Animals received 0.5 μl/hr of vehicle or compound for 1 week [39-41]. Therefore, the doses of BzATP, OxATP and IL-1Ra were 43 μg, 30 μg and 0.06 μg/day per animal, respectively.…”

Section: Methodsmentioning

confidence: 99%

P2X7 receptor regulates leukocyte infiltrations in rat frontoparietal cortex following status epilepticus

Kim

Ryu

Yeo

et al. 2010

J Neuroinflammation

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BackgroundIn the present study, we investigated the roles of P2X7 receptor in recruitment and infiltration of neutrophil during epileptogenesis in rat epilepsy models.MethodsStatus epilepticus (SE) was induced by pilocarpine in rats that were intracerebroventricularly infused with either saline, 2',3'-O-(4-benzoylbenzoyl)-adenosine 5'-triphosphate (BzATP), adenosine 5'-triphosphate-2',3'-dialdehyde (OxATP), or IL-1Ra (interleukin 1 receptor antagonist) prior to SE induction. Thereafter, we performed immunohistochemical studies for myeloperoxidase (MPO), CD68, interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2).ResultsIn saline-infused animals, neutrophils and monocytes were observed in frontoparietal cortex (FPC) at 1 day and 2 days after SE, respectively. In BzATP-infused animals, infiltrations of neutrophils and monocytes into the FPC were detected at 12 hr and 1 day after SE, respectively. In OxATP-infused animals, neutrophils and monocytes infiltrated into the FPC at 1 day and 2 days after SE, respectively. However, the numbers of both classes of leukocytes were significantly lower than those observed in the saline-infused group. In piriform cortex (PC), massive leukocyte infiltration was detected in layers III/IV of saline-infused animals at 1-4 days after induction of SE. BzATP or OxATP infusion did not affect neutrophil infiltration in the PC. In addition, P2X7 receptor-mediated MCP-1 (released from microglia)/MIP-2 (released from astrocytes) regulation was related to SE-induced leukocyte infiltration in an IL-1β-independent manner.ConclusionsOur findings suggest that selective regulation of P2X7 receptor-mediated neutrophil infiltration may provide new therapeutic approaches to SE or epilepsy.

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The protective effects of interleukin-18 and interferon-γ on neuronal damages in the rat hippocampus following status epilepticus

Cited by 36 publications

References 52 publications

FAAH-mediated modulation of TLR3-induced neuroinflammation in the rat hippocampus

FAAH-mediated modulation of TLR3-induced neuroinflammation in the rat hippocampus

Increased tryptophan transport in epileptogenic dysembryoplastic neuroepithelial tumors

P2X7 receptor regulates leukocyte infiltrations in rat frontoparietal cortex following status epilepticus

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