Cytokines and Neurodegeneration in Epileptogenesis
Epilepsy is a common brain disorder characterized by a heterogenous etiology. Its main features are recurrent seizures. Despite many clinical studies, about 30% of cases are refractory to treatment. Recent studies suggested the important role of immune-system elements in its pathogenesis. It was sug...
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MDPI AG
2022-03-01
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Series: | Brain Sciences |
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Online Access: | https://www.mdpi.com/2076-3425/12/3/380 |
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author | Pawel Wolinski Dominika Ksiazek-Winiarek Andrzej Glabinski |
author_facet | Pawel Wolinski Dominika Ksiazek-Winiarek Andrzej Glabinski |
author_sort | Pawel Wolinski |
collection | DOAJ |
description | Epilepsy is a common brain disorder characterized by a heterogenous etiology. Its main features are recurrent seizures. Despite many clinical studies, about 30% of cases are refractory to treatment. Recent studies suggested the important role of immune-system elements in its pathogenesis. It was suggested that a deregulated inflammatory process may lead to aberrant neural connectivity and the hyperexcitability of the neuronal network. The aim of our study was the analysis of the expression of inflammatory mediators in a mouse model of epilepsy and their impact on the neurodegeneration process located in the brain. We used the KA-induced model of epilepsy in SJL/J mice and performed the analysis of gene expression and protein levels. We observed the upregulation of IL1β and CXCL12 in the early phase of KA-induced epilepsy and elevated levels of CCL5 at a later time point, compared with control animals. The most important result obtained in our study is the elevation of CXCL2 expression at both studied time points and its correlation with the neurodegeneration observed in mouse brain. Increasing experimental and clinical data suggest the influence of peripheral inflammation on epileptogenesis. Thus, studies focused on the molecular markers of neuroinflammation are of great value and may help deepen our knowledge about epilepsy, leading to the discovery of new drugs. |
first_indexed | 2024-03-09T13:49:24Z |
format | Article |
id | doaj.art-b4501f969f7847f184de522db781cf06 |
institution | Directory Open Access Journal |
issn | 2076-3425 |
language | English |
last_indexed | 2024-03-09T13:49:24Z |
publishDate | 2022-03-01 |
publisher | MDPI AG |
record_format | Article |
series | Brain Sciences |
spelling | doaj.art-b4501f969f7847f184de522db781cf062023-11-30T20:54:07ZengMDPI AGBrain Sciences2076-34252022-03-0112338010.3390/brainsci12030380Cytokines and Neurodegeneration in EpileptogenesisPawel Wolinski0Dominika Ksiazek-Winiarek1Andrzej Glabinski2Department of Neurology and Stroke, Medical University of Lodz, 90-549 Lodz, PolandDepartment of Neurology and Stroke, Medical University of Lodz, 90-549 Lodz, PolandDepartment of Neurology and Stroke, Medical University of Lodz, 90-549 Lodz, PolandEpilepsy is a common brain disorder characterized by a heterogenous etiology. Its main features are recurrent seizures. Despite many clinical studies, about 30% of cases are refractory to treatment. Recent studies suggested the important role of immune-system elements in its pathogenesis. It was suggested that a deregulated inflammatory process may lead to aberrant neural connectivity and the hyperexcitability of the neuronal network. The aim of our study was the analysis of the expression of inflammatory mediators in a mouse model of epilepsy and their impact on the neurodegeneration process located in the brain. We used the KA-induced model of epilepsy in SJL/J mice and performed the analysis of gene expression and protein levels. We observed the upregulation of IL1β and CXCL12 in the early phase of KA-induced epilepsy and elevated levels of CCL5 at a later time point, compared with control animals. The most important result obtained in our study is the elevation of CXCL2 expression at both studied time points and its correlation with the neurodegeneration observed in mouse brain. Increasing experimental and clinical data suggest the influence of peripheral inflammation on epileptogenesis. Thus, studies focused on the molecular markers of neuroinflammation are of great value and may help deepen our knowledge about epilepsy, leading to the discovery of new drugs.https://www.mdpi.com/2076-3425/12/3/380epilepsyIL1βCXCL2CXCL12CCL5kainic-acid epilepsy model |
spellingShingle | Pawel Wolinski Dominika Ksiazek-Winiarek Andrzej Glabinski Cytokines and Neurodegeneration in Epileptogenesis Brain Sciences epilepsy IL1β CXCL2 CXCL12 CCL5 kainic-acid epilepsy model |
title | Cytokines and Neurodegeneration in Epileptogenesis |
title_full | Cytokines and Neurodegeneration in Epileptogenesis |
title_fullStr | Cytokines and Neurodegeneration in Epileptogenesis |
title_full_unstemmed | Cytokines and Neurodegeneration in Epileptogenesis |
title_short | Cytokines and Neurodegeneration in Epileptogenesis |
title_sort | cytokines and neurodegeneration in epileptogenesis |
topic | epilepsy IL1β CXCL2 CXCL12 CCL5 kainic-acid epilepsy model |
url | https://www.mdpi.com/2076-3425/12/3/380 |
work_keys_str_mv | AT pawelwolinski cytokinesandneurodegenerationinepileptogenesis AT dominikaksiazekwiniarek cytokinesandneurodegenerationinepileptogenesis AT andrzejglabinski cytokinesandneurodegenerationinepileptogenesis |