Adoptive transfer of T lymphocytes in immunodeficient mice influences epileptogenesis and neurodegeneration in a model of temporal lobe epilepsy

Deprez, Francine; Zattoni, Michela; Mura, Maria Luisa; Frei, Karl; Fritschy, Jean‐Marc

doi:10.1016/j.nbd.2011.06.011

Cited by 26 publications

(32 citation statements)

References 32 publications

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“…Similarly, Zattoni et al [7] depleted peripheral monocytes through intraperitoneal administration of clodronate liposomes to block the origin of infiltrated macrophages; and results showed that the number of infiltrated F4/80 ? macrophages was remarkably reduced; besides, depletion of these cells markedly worsened KA-lesion and induced granule cell degeneration, corroborated by other animal studies [50,55,60] suggesting a significant promotion of macrophage on granule cell survival. In summary, infiltrated macrophages are peripheral origin; in addition, they prevent degeneration of granule cell and neuron in animal models, regardless of its pro-inflammation capacity during epileptogenesis.…”

Section: Monocytes/macrophagessupporting

confidence: 81%

“…Histopathological detection in this study revealed the fewest pathological changes in CD4/CD8 (-/-) mice 7 days after KA-infusion [43]. Besides, Deprez's [55] and Zattoni's [7] studies also showed advanced spontaneous recurrent seizures (SRS) onset and delayed hippocampal destruction by neutrophils in RAG1-KO mice, indicating a neuroprotective role of T cells infiltrated in the epileptic focus. Besides, Deprez and Zattoni et al [55] also demonstrated that an intact adaptive immunity was necessary for delayed SRS onset, as MHCIIknock-out (lacking CD4 ?…”

Section: T Cellsmentioning

confidence: 52%

“…and CD4 ? T cells to the pathogenesis and pathology of epilepsy, Deprez et al [55] transferred CD4 ? and CD8 ?…”

Section: T Cellsmentioning

confidence: 99%

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Some cross-talks between immune cells and epilepsy should not be forgotten

et al. 2014

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Recent studies have reported that immune cells were not always found in brain specimens from epileptic patients, then should we stop investigating the relationship between these cells and epilepsy? The answer is no! In addition to immunocyte infiltration in brain parenchyma, a flurry of papers have demonstrated that there were significant alterations in peripheral blood cells (PBCs) immediately after seizure onset, especially changes in some specific transporters of neurotransmitters expressed on the membrane of immunocyte. These transporters may regulate neuronal excitability in mature neurons. Besides, many researchers did find activated leukocytes adhered to the endothelium of blood brain barrier or infiltrated into the brain parenchyma in several types of epilepsy both in human and animal studies; moreover, it is worth noting that different immune cells play different roles in epilepsy development, which was indicated by in vitro and in vivo evidence. This review is going to summarize available evidence supporting changes in PBCs after seizures, and will also focus on some specific effects of immune cells on epilepsy development.

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Section: Monocytes/macrophagessupporting

confidence: 81%

Section: T Cellsmentioning

confidence: 52%

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Some cross-talks between immune cells and epilepsy should not be forgotten

et al. 2014

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“…It is suspected that the kainate has a tropism for the hippocampus, which led several authors to consider that the kainate induces specifically a HS. Yet, the mechanisms by which kainate induces an epileptic activity is still debated; the immune system and leakage of the blood–brain barrier have been cited as critical for the expression of the disease (233, 234). Hence, it is not excluded that systemic kainate may have diffuse effects on the brain.…”

Section: What We Can Learn From Animal Modelsmentioning

confidence: 99%

Mapping Epileptic Activity: Sources or Networks for the Clinicians?

Pittau¹,

Mégevand

Sheybani

et al. 2014

Front. Neurol.

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Epileptic seizures of focal origin are classically considered to arise from a focal epileptogenic zone and then spread to other brain regions. This is a key concept for semiological electro-clinical correlations, localization of relevant structural lesions, and selection of patients for epilepsy surgery. Recent development in neuro-imaging and electro-physiology and combinations, thereof, have been validated as contributory tools for focus localization. In parallel, these techniques have revealed that widespread networks of brain regions, rather than a single epileptogenic region, are implicated in focal epileptic activity. Sophisticated multimodal imaging and analysis strategies of brain connectivity patterns have been developed to characterize the spatio-temporal relationships within these networks by combining the strength of both techniques to optimize spatial and temporal resolution with whole-brain coverage and directional connectivity. In this paper, we review the potential clinical contribution of these functional mapping techniques as well as invasive electrophysiology in human beings and animal models for characterizing network connectivity.

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“…In particular, high levels of proinflammatory cytokines [e.g., interleukin-1beta (IL-1β), tumor necrosis factor-alpha (TNFα)], damage signals [high-mobility group box 1 (HMGB1), S100 beta] and downstream inflammatory mediators (e.g., prostaglandins, the complement system) have been measured in epileptogenic tissue from patients affected by epilepsy of various etiologies (Aronica and Crino, 2011; Vezzani et al, 2011). The major contributors to the synthesis of these inflammatory mediators are brain-resident cells such as activated microglia, astrocytes, and neurons (Devinsky et al, 2013), but also systemic invading leukocytes play an important role in epileptogenesis, particularly when the permeability of the blood-brain barrier is alterated (Fabene et al, 2008; Deprez et al, 2011). …”

Section: Introductionmentioning

confidence: 99%

The inflammatory molecules IL-1Î² and HMGB1 can rapidly enhance focal seizure generation in a brain slice model of temporal lobe epilepsy

Chiavegato

Zurolo

Losi

et al. 2014

Front. Cell. Neurosci.

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Epilepsy is a neurological disorder characterized by a hyperexcitable brain tissue and unpredictable seizures, i.e., aberrant firing discharges in large neuronal populations. It is well established that proinflammatory cytokines, in addition to their canonical involvement in the immune response, have a crucial role in the mechanism of seizure generation. The purpose of the present study was to investigate the role of interleukin-1β (IL-1β) and high mobility group B1 (HMGB1) in the generation of seizure-like discharges using two models of focal epilepsy in a rat entorhinal cortex slice preparation. Seizure like-discharges were evoked by either slice perfusion with low Mg2+ and picrotoxin or with a double NMDA local stimulation in the presence of the proconvulsant 4-amino-pyridine. The effects of IL-1β or HMGB1 were evaluated by monitoring seizure discharge generation through laser scanning microscope imaging of Ca2+ signals from neurons and astrocytes. In the picrotoxin model, we revealed that both cytokines increased the mean frequency of spontaneous ictal-like discharges, whereas only IL-1β reduced the latency and prolonged the duration of the first ictal-like event. In the second model, a single NMDA pulse, per se ineffective, became successful when it was performed after IL-β or HMGB1 local applications. These findings demonstrate that both IL-1β and HMGB1 can rapidly lower focal ictal event threshold and strengthen the possibility that targeting these inflammatory pathways may represent an effective therapeutic strategy to prevent seizures.

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Adoptive transfer of T lymphocytes in immunodeficient mice influences epileptogenesis and neurodegeneration in a model of temporal lobe epilepsy

Cited by 26 publications

References 32 publications

Some cross-talks between immune cells and epilepsy should not be forgotten

Some cross-talks between immune cells and epilepsy should not be forgotten

Mapping Epileptic Activity: Sources or Networks for the Clinicians?

The inflammatory molecules IL-1Î² and HMGB1 can rapidly enhance focal seizure generation in a brain slice model of temporal lobe epilepsy

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