Interleukin-18 attenuates disruption of brain-blood barrier induced by status epilepticus within the rat piriform cortex in interferon-gamma independent pathway.

Authors: Jung, HK  Ryu, HJ  Kim, MJ  Kim, WI  Choi, HK  Choi, HC  Song, HK  Jo, SM  Kang, TC 
Citation: Jung HK, etal., Brain Res. 2012 Apr 4;1447:126-34. Epub 2012 Jan 31.
Pubmed: (View Article at PubMed) PMID:22338606
DOI: Full-text: DOI:10.1016/j.brainres.2012.01.057

Status epilepticus increases brain-blood barrier (BBB) permeability leading to vasogenic edema. This BBB disruption is usually confined within relatively limited cerebral regions including the piriform cortex (PC), and leads to epileptogenesis and contributes to progression of epilepsy. Although cytokines are at least partly responsible for changes in BBB permeability, the role of interleukin-18 (IL-18) in vasogenic edema is not yet explored in detail. In the present study, we investigated the role of IL-18 in SE-induced vasogenic edema formation. Following SE, IL-18/interferon-gamma (IFN-gamma) system was up-regulated in astrocytes and microglia/macrophages. Recombinant rat (rr) IL-18 infusion decreased vasogenic edema formation, while anti-rat IL-18 infusion increased it. In contrast, rrIFN-gamma, and anti-rat IFN-gamma infusion showed reverse effects on vasogenic edema formation. rrIL-18 or anti-rat IFN-gamma IgG infusion elevated dystrophin expression accompanied by the reduction in vasogenic edema. However, rr-IFN-gamma or anti-rat IL-18 IgG infusion significantly decreased dystrophin immunoreactivity within the PC following SE. These findings indicate that IL-18-mediated up-regulation of dystrophin expression may play either a direct or indirect role in maintenance of BBB function following SE. Therefore, our findings suggest that IL-18 may have protective effect on SE-induced BBB disruption in IFN-gamma independent mechanism.


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CRRD Object Information
CRRD ID: 6771363
Created: 2012-07-30
Species: All species
Last Modified: 2012-07-30
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.