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Interleukin-18 expression increases in response to neurovascular damage following soman-induced status epilepticus in rats

Overview of attention for article published in Journal of Inflammation, July 2015
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Title
Interleukin-18 expression increases in response to neurovascular damage following soman-induced status epilepticus in rats
Published in
Journal of Inflammation, July 2015
DOI 10.1186/s12950-015-0089-9
Pubmed ID
Authors

Erik A. Johnson, Michelle A. Guignet, Thuy L. Dao, Tracey A. Hamilton, Robert K. Kan

Abstract

Status epilepticus (SE) can cause neuronal cell death and impaired behavioral function. Acute exposure to potent acetylcholinesterase inhibitors such as soman (GD) can cause prolonged SE activity, micro-hemorrhage and cell death in the hippocampus, thalamus and piriform cortex. Neuroinflammation is a prominent feature of brain injury with upregulation of multiple pro-inflammatory cytokines including those of the IL-1 family. The highly pleiotropic pro-inflammatory cytokine interleukin-18 (IL-18) belongs to the IL-1 family of cytokines and can propagate neuroinflammation by promoting immune cell infiltration, leukocyte and lymphocyte activation, and angiogenesis and helps facilitate the transition from the innate to the adaptive immune response. The purpose of this study is to characterize the regional and temporal expression of IL -18 and related factors in the brain following SE in a rat GD seizure model followed by localization of IL-18 to specific cell types. The protein levels of IL-18, vascular endothelial growth factor and interferon gamma was quantified in the lysates of injured brain regions up to 72 h following GD-induced SE onset using bead multiplex immunoassays. IL-18 was localized to various cell types using immunohistochemistry and transmission electron microscopy. In addition, macrophage appearance scoring and T-cell quantification was determined using immunohistochemistry. Micro-hemorrhages were identified using hematoxylin and eosin staining of brain sections. Significant increases in IL-18 occurred in the piriform cortex, hippocampus and thalamus following SE. IL-18 was primarily expressed by endothelial cells and astrocytes associated with the damaged neurovascular unit. The increase in IL-18 was not related to macrophage accumulation, neutrophil infiltration or T-cell appearance in the injured tissue. These data show that IL-18 is significantly upregulated following GD-induced SE and localized primarily to endothelial cells in damaged brain vasculature. IL-18 upregulation occurred following leukocyte/lymphocyte infiltration and in the absence of other IL-18-related cytokines, suggesting another function, potentially for angiogenesis related to GD-induced micro-hemorrhage formation. Further studies at more chronic time points may help to elucidate this function.

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The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 5 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Mexico 1 20%
Unknown 4 80%

Demographic breakdown

Readers by professional status Count As %
Student > Master 3 60%
Student > Postgraduate 1 20%
Other 1 20%
Readers by discipline Count As %
Agricultural and Biological Sciences 1 20%
Physics and Astronomy 1 20%
Neuroscience 1 20%
Medicine and Dentistry 1 20%
Unknown 1 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 July 2015.
All research outputs
#3,790,516
of 5,387,274 outputs
Outputs from Journal of Inflammation
#98
of 149 outputs
Outputs of similar age
#131,887
of 190,078 outputs
Outputs of similar age from Journal of Inflammation
#8
of 8 outputs
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So far Altmetric has tracked 149 research outputs from this source. They receive a mean Attention Score of 2.3. This one is in the 14th percentile – i.e., 14% of its peers scored the same or lower than it.
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