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The interaction between brain inflammation and systemic infection

The interaction between brain inflammation and systemic infection
The interaction between brain inflammation and systemic infection
In this chapter we consider the biological mechanisms underlying central cytokine expression, discuss their physiological relevance in the context of systemic inflammation, and contemplate the recent evidence demonstrating that pro-inflammatory cytokines can exacerbate neuronal death and inflammation in rodent models of CNS disease. We also describe the bi-directional nature of communication between the CNS and peripheral immune system, placing particular emphasis on the acute phase response to brain injury, and the complex role of the liver. In order to provide a comprehensive review, we have focused on a number of pro- and anti-inflammatory cytokines, chemokines, and lipophilic mediators of inflammation; and describe how their expression may exacerbate tissue injury in acute brain injury, multiple sclerosis (MS), and chronic neurodegenerative disease (prion diseases, Alzheimer's disease). We also describe the impact of repeated systemic infection on the immunological status of the mammalian CNS, and summarize evidence demonstrating that priming of microglia, and other glia, by prolonged or repeated exposure to pro-inflammatory mediators can impact on the progression, severity, and clinical expression of subsequent CNS disease.
429-448
Academic Press
Felton, Leigh M.
a32ee02f-0da4-45d0-81fc-32ac7839c1e6
Perry, V. Hugh
8f29d36a-8e1f-4082-8700-09483bbaeae4
Ader, Robert
Felton, Leigh M.
a32ee02f-0da4-45d0-81fc-32ac7839c1e6
Perry, V. Hugh
8f29d36a-8e1f-4082-8700-09483bbaeae4
Ader, Robert

Felton, Leigh M. and Perry, V. Hugh (2007) The interaction between brain inflammation and systemic infection. In, Ader, Robert (ed.) Psychoneuroimmunology. 4 ed. Academic Press, pp. 429-448. (doi:10.1016/B978-012088576-3/50025-3).

Record type: Book Section

Abstract

In this chapter we consider the biological mechanisms underlying central cytokine expression, discuss their physiological relevance in the context of systemic inflammation, and contemplate the recent evidence demonstrating that pro-inflammatory cytokines can exacerbate neuronal death and inflammation in rodent models of CNS disease. We also describe the bi-directional nature of communication between the CNS and peripheral immune system, placing particular emphasis on the acute phase response to brain injury, and the complex role of the liver. In order to provide a comprehensive review, we have focused on a number of pro- and anti-inflammatory cytokines, chemokines, and lipophilic mediators of inflammation; and describe how their expression may exacerbate tissue injury in acute brain injury, multiple sclerosis (MS), and chronic neurodegenerative disease (prion diseases, Alzheimer's disease). We also describe the impact of repeated systemic infection on the immunological status of the mammalian CNS, and summarize evidence demonstrating that priming of microglia, and other glia, by prolonged or repeated exposure to pro-inflammatory mediators can impact on the progression, severity, and clinical expression of subsequent CNS disease.

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e-pub ahead of print date: 28 September 2007
Published date: 2007

Identifiers

Local EPrints ID: 489485
URI: http://eprints.soton.ac.uk/id/eprint/489485
PURE UUID: ab4d111e-f88b-4ef3-9c17-ea718366da2a

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Date deposited: 25 Apr 2024 16:32
Last modified: 05 Jun 2024 20:05

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Contributors

Author: Leigh M. Felton
Author: V. Hugh Perry
Editor: Robert Ader

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