The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations

<p>Abstract</p> <p>Background</p> <p>Neuroinflammation occurs following brain injury, including soman (GD) induced status epilepticus (SE), and may contribute to loss of neural tissue and declined behavioral function. However, little is known about this important pathol...

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Main Authors: Kan Robert K, Johnson Erik A
Format: Article
Language:English
Published: BMC 2010-07-01
Series:Journal of Neuroinflammation
Online Access:http://www.jneuroinflammation.com/content/7/1/40
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spelling doaj-7dc53aa3cc614be88d0c4dfe5931b9752020-11-24T21:58:25ZengBMCJournal of Neuroinflammation1742-20942010-07-01714010.1186/1742-2094-7-40The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrationsKan Robert KJohnson Erik A<p>Abstract</p> <p>Background</p> <p>Neuroinflammation occurs following brain injury, including soman (GD) induced status epilepticus (SE), and may contribute to loss of neural tissue and declined behavioral function. However, little is known about this important pathological process following GD exposure. Limited transcriptional information on a small number of brain-expressed inflammatory mediators has been shown following GD-induced SE and even less information on protein upregulation has been elucidated. The purpose of this study is to further characterize the regional and temporal progression of the neuroinflammatory process following acute GD-induced SE.</p> <p>Methods</p> <p>The protein levels of 10 cytokines was quantified using bead multiplex immunoassays in damaged brain regions (i.e., piriform cortex, hippocampus and thalamus) up to 72 hours following seizure onset. Those factors showing significant changes were then localized to neural cells using fluorescent IHC.</p> <p>Results</p> <p>A significant concentration increase was observed in all injured brain regions for four acute phase response (APR) induction cytokines: interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor (TNF)-α. Increases in these APR cytokines corresponded both temporally and regionally to areas of known seizure damage and neuronal death. Neurotoxic cytokines IL-1α and IL-1β were primarily expressed by activated microglia whereas the potentially neuroprotective cytokine IL-6 was expressed by neurons and hypertrophic astrocytes.</p> <p>Conclusions</p> <p>Increases in neurotoxic cytokines likely play an active role in the progression of GD-induced SE neuropathology though the exact role that these and other cytokines play in this process require further study.</p> http://www.jneuroinflammation.com/content/7/1/40
collection DOAJ
language English
format Article
sources DOAJ
author Kan Robert K
Johnson Erik A
spellingShingle Kan Robert K
Johnson Erik A
The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
Journal of Neuroinflammation
author_facet Kan Robert K
Johnson Erik A
author_sort Kan Robert K
title The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
title_short The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
title_full The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
title_fullStr The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
title_full_unstemmed The acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
title_sort acute phase response and soman-induced status epilepticus: temporal, regional and cellular changes in rat brain cytokine concentrations
publisher BMC
series Journal of Neuroinflammation
issn 1742-2094
publishDate 2010-07-01
description <p>Abstract</p> <p>Background</p> <p>Neuroinflammation occurs following brain injury, including soman (GD) induced status epilepticus (SE), and may contribute to loss of neural tissue and declined behavioral function. However, little is known about this important pathological process following GD exposure. Limited transcriptional information on a small number of brain-expressed inflammatory mediators has been shown following GD-induced SE and even less information on protein upregulation has been elucidated. The purpose of this study is to further characterize the regional and temporal progression of the neuroinflammatory process following acute GD-induced SE.</p> <p>Methods</p> <p>The protein levels of 10 cytokines was quantified using bead multiplex immunoassays in damaged brain regions (i.e., piriform cortex, hippocampus and thalamus) up to 72 hours following seizure onset. Those factors showing significant changes were then localized to neural cells using fluorescent IHC.</p> <p>Results</p> <p>A significant concentration increase was observed in all injured brain regions for four acute phase response (APR) induction cytokines: interleukin (IL)-1α, IL-1β, IL-6, and tumor necrosis factor (TNF)-α. Increases in these APR cytokines corresponded both temporally and regionally to areas of known seizure damage and neuronal death. Neurotoxic cytokines IL-1α and IL-1β were primarily expressed by activated microglia whereas the potentially neuroprotective cytokine IL-6 was expressed by neurons and hypertrophic astrocytes.</p> <p>Conclusions</p> <p>Increases in neurotoxic cytokines likely play an active role in the progression of GD-induced SE neuropathology though the exact role that these and other cytokines play in this process require further study.</p>
url http://www.jneuroinflammation.com/content/7/1/40
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