Moynagh, Paul N. (2005) The interleukin-1 signalling pathway in astrocytes: a key contributor to inflammation in the brain. Journal of Anatomy, 207 (3). pp. 265-269. ISSN 0021-8782

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Abstract

A dysregulated inflammatory response in the central nervous system (CNS) lies at the heart of many neuropathological conditions such as multiple sclerosis and Alzheimer’s disease. A key component of these inflammatory conditions is the accumulation of leukocytes in the CNS. The infiltration of leukocytes into the brain is dependent on the induction of leukocyte adhesion molecules and chemoattractant chemokines. Recent studies have suggested the astrocyte to be a key cell in mediating the inflammatory process in the brain and in expressing adhesion molecules and chemokines. Here I overview work in my laboratory and others that demonstrates interleukin-1 (IL- 1) to be a key inducer of the expression of these molecules in astrocytes. The temporal expression is sustained in nature and this is due to prolonged activation of the transcription factor NFκB. The molecular basis to the sustained activation of NFκB is also discussed. The IL-1 signalling pathway thus emerges as a valuable therapeutic target in the treatment of presently incurable neuropathological conditions.

Item Type:	Article
Additional Information:	This publication emanated from research conducted with the financial support of Science Foundation Ireland, Health Research Board of Ireland and Higher Education Authority of Ireland.
Keywords:	adhesion molecules; astrocytes; interleukin-1; neuroinflammation; NF-κB.;
Academic Unit:	Faculty of Science and Engineering > Biology
Item ID:	7193
Identification Number:	https://doi.org/10.1111/j.1469-7580.2005.00445.x
Depositing User:	Professor Paul Moynagh
Date Deposited:	18 Jul 2016 09:10
Journal or Publication Title:	Journal of Anatomy
Publisher:	Anatomical Society of Great Britain and Ireland
Refereed:	Yes
Funders:	Science Foundation Ireland (SFI), Health Research Board (HRB), Higher Education Authority (HEA)
URI:
Use Licence:	This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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