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Absence of detectable IL-1 beta production in murine prion disease: A model of chronic neurodegeneration

Walsh, D.T., Betmouni, S. and Perry, V.H. (2001) Absence of detectable IL-1 beta production in murine prion disease: A model of chronic neurodegeneration Journal of Neuropathology and Experimental Neurology, 60, (2), pp. 173-182.

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Murine prion disease is accompanied by a modified inflammatory response characterized by early but prolonged microglial activation and T-lymphocyte recruitment. In this model, we look at the profile of cytokine production, particularly IL-1[beta]. Mice inoculated with prion-infected brain homogenate show typical signs of prion disease. We were unable to detect any IL-1[beta] using immunohistochemistry, with various fixation protocols, or ELISA between 8 and 24 wk post-inoculation. Also, there was no increase in mRNA for IL-1[beta], IL-6, IFN[gamma], and iNOS as measured by quantitative RT-PCR. Using the same procedures and examining tissues at the same time, IL-1[beta] immunostaining was detected in infiltrating inflammatory cells in mouse brains injected with LPS or in a delayed-type hypersensitivity response in the brain. Soluble IL-1[beta] was also increased, as measured by ELISA, and there was an increase in mRNA species for IL-1[beta], IL-6, TNF[alpha] but not IFN[gamma] or iNOS in these brains. These data reveal that chronic neurodegeneration seen in prion disease does not induce production of a range of proinflammatory mediators despite showing marked microglial activation and raise the question as to whether IL-1[beta] would exacerbate the neurodegeneration as it does in acute neurodegeneration following head injury and stroke.

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Published date: February 2001
Organisations: Biological Sciences


Local EPrints ID: 56490
ISSN: 0022-3069
PURE UUID: f4d77153-d3c1-4a05-be07-890936dabcef

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Date deposited: 08 Aug 2008
Last modified: 17 Jul 2017 14:30

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Author: D.T. Walsh
Author: S. Betmouni
Author: V.H. Perry

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