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Transgenic Inhibition of Astroglial NF-kappa B Improves Functional Outcome in Experimental Autoimmune Encephalomyelitis by Suppressing Chronic Central Nervous System Inflammation
Journal article   Open access   Peer reviewed

Transgenic Inhibition of Astroglial NF-kappa B Improves Functional Outcome in Experimental Autoimmune Encephalomyelitis by Suppressing Chronic Central Nervous System Inflammation

Roberta Brambilla, Trikaldarshi Persaud, Xianchen Hu, Shaffiat Karmally, Valery I. Shestopalov, Galina Dvoriantchikova, Dmitry Ivanov, Lubov Nathanson, Scott R. Barnum and John R. Bethea
The Journal of immunology (1950), v 182(5), pp 2628-2640
01 Mar 2009
PMID: 19234157
url
http://www.jimmunol.org/content/182/5/2628.full.pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.4049/jimmunol.0802954View
Published, Version of Record (VoR) Open

Abstract

Immunology Life Sciences & Biomedicine Science & Technology
In the CNS, the transcription factor NF-kappa B is a key regulator of inflammation and secondary injury processes. Following trauma protective and detrimental effects. In this study, or disease, the expression of NF-kappa B-dependent genes is activated, leading to both pro we show that transgenic inactivation of astroglial NF-kappa B (glial fibrillary acidic protein-I kappa B alpha-dominant-negative mice) resulted in reduced disease severity and improved functional recovery following experimental autoimmune encephalomyelitis. At the chronic stage of the disease, transgenic mice exhibited an overall higher presence of leukocytes in spinal cord and brain, and a markedly higher percentage of CD8(+)CD122(+) T regulatory cells compared with wild type, which correlated with the timing of clinical recovery. We also observed that expression of proinflammatory genes in both spinal cord and cerebellum was delayed and reduced, whereas the loss of neuronal-specific molecules essential for synaptic transmission was limited compared with wild-type mice. Furthermore, death of retinal ganglion cells in affected retinas was almost abolished, suggesting the activation of neuroprotective mechanisms. Our data indicate that inhibiting NF-kappa B in astrocytes results in neuroprotective effects following experimental autoimmune encephalomyelitis, directly implicating astrocytes in the pathophysiology of this disease. The Journal of Immunology, 2009, 182: 2628-2640.

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Immunology
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