Atypical inflammation in the central nervous system in prion disease
Atypical inflammation in the central nervous system in prion disease
The inflammatory response in prion diseases is dominated by microglial activation. Contrary to their profile in vitro none of the pro-inflammatory cytokines interleukin-1[beta], interleukin-6, or tumour necrosis factor-[alpha] are significantly upregulated in the ME7 model of prion disease. However, two major inflammatory mediators are elevated: transforming growth factor-[beta]1 and prostaglandin E2. This cytokine profile is the same as that reported for macrophages during phagocytosis of apoptotic cells and indeed transforming growth factor-[beta]1 and prostaglandin E2 are responsible for the downregulated phenotype of these macrophages. Transforming growth factor-[beta]1 may also have roles in extracellular matrix deposition and in amyloidogenesis and may play a direct role in disease pathogenesis. There is also now evidence to suggest that a peripheral infection, and its consequent systemic cytokine expression, may drive central nervous system cytokine expression and perhaps exacerbate disease.
349-354
Perry, VH.
8f29d36a-8e1f-4082-8700-09483bbaeae4
Cunningham, C.
6d675038-a4b1-46e2-9e4b-0a5ac27ea2b2
Boche, D.
bdcca10e-6302-4dd0-919f-67218f7e0d61
June 2002
Perry, VH.
8f29d36a-8e1f-4082-8700-09483bbaeae4
Cunningham, C.
6d675038-a4b1-46e2-9e4b-0a5ac27ea2b2
Boche, D.
bdcca10e-6302-4dd0-919f-67218f7e0d61
Perry, VH., Cunningham, C. and Boche, D.
(2002)
Atypical inflammation in the central nervous system in prion disease.
Current Opinion in Neurology, 15 (3), .
Abstract
The inflammatory response in prion diseases is dominated by microglial activation. Contrary to their profile in vitro none of the pro-inflammatory cytokines interleukin-1[beta], interleukin-6, or tumour necrosis factor-[alpha] are significantly upregulated in the ME7 model of prion disease. However, two major inflammatory mediators are elevated: transforming growth factor-[beta]1 and prostaglandin E2. This cytokine profile is the same as that reported for macrophages during phagocytosis of apoptotic cells and indeed transforming growth factor-[beta]1 and prostaglandin E2 are responsible for the downregulated phenotype of these macrophages. Transforming growth factor-[beta]1 may also have roles in extracellular matrix deposition and in amyloidogenesis and may play a direct role in disease pathogenesis. There is also now evidence to suggest that a peripheral infection, and its consequent systemic cytokine expression, may drive central nervous system cytokine expression and perhaps exacerbate disease.
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Published date: June 2002
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Local EPrints ID: 27683
URI: http://eprints.soton.ac.uk/id/eprint/27683
ISSN: 1350-7540
PURE UUID: 064669c4-f747-46b8-8a68-7972e00660f8
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Date deposited: 25 Apr 2006
Last modified: 27 Apr 2022 01:42
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C. Cunningham
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