NR AJJW
AU Perry,V.H.; Cunningham,C.; Boche,D.
TI Atypical inflammation in the central nervous system in prion disease
QU Current Opinion in Neurology 2002 Jun; 15(3): 349-54
PT journal article; review; review, tutorial
AB The inflammatory response in prion diseases is dominated by microglial activation. Contrary to their profile in vitro none of the pro-inflammatory cytokines interleukin-1ß, 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-beta1 and prostaglandin E2. This cytokine profile is the same as that reported for macrophages during phagocytosis of apoptotic cells and indeed transforming growth factor-beta1 and prostaglandin E2 are responsible for the downregulated phenotype of these macrophages. Transforming growth factor-beta1 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.
ZR 65
MH Animal; Central Nervous System/*immunology/metabolism/physiopathology; Cytokines/*immunology/metabolism; Dinoprostone/immunology; Encephalitis/*immunology/metabolism/physiopathology; Human; Microglia/cytology/*immunology/metabolism; Prion Diseases/*immunology/metabolism/physiopathology; Reactive Oxygen Species/immunology; Transforming Growth Factor beta/immunology
AD CNS Inflammation Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK. vhp@soton.ac.uk
SP englisch
PO England