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60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

German Society for Neuropathology and Neuroanatomy

26. - 28.08.2015, Berlin

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Interleukin-10 receptor blockade enhances neuroinflammation in Theiler’s murine encephalomyelitis

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  • corresponding author Ann-Kathrin Uhde - Department of Pathology, TiHo Hannover, Hanover, Germany
  • Vanessa Herder - Department of Pathology, TiHo Hannover, Hanover, Germany
  • Rene Teich - Department of Experimental Immunology, HZI Braunschweig, Braunschweig, Germany
  • Stefan Flöß - Department of Experimental Immunology, HZI Braunschweig, Braunschweig, Germany
  • Wolfgang Baumgärtner - Department of Pathology, TiHo Hannover, Hanover, Germany
  • Jochen Huehn - Department of Experimental Immunology, HZI Braunschweig, Braunschweig, Germany
  • presenting/speaker Andreas Beineke - Department of Pathology, TiHo Hannover, Hanover, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 60th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Berlin, 26.-28.08.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15dgnnP25

doi: 10.3205/15dgnn49, urn:nbn:de:0183-15dgnn497

Published: August 25, 2015

© 2015 Uhde et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.

Outline

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Introduction: Theiler’s murine encephalomyelitis (TME) serves as an important model for acute and chronic infectious disorders of the central nervous system (CNS). In the present study the influence of interleukin (IL)-10 pathway modulation upon neuropathology was investigated in TME virus-infected SJL mice.

Materials and methods: Five week old SJL mice were intracerebrally infected with TME virus and treated with IL-10 receptor-blocking antibodies (anti-IL-10R Ab) or isotype control. At necropsy brains and spinal cords were examined by histology, immunohistochemistry and reverse transcriptase polymerase chain reaction. Phenotypical changes in lymphoid organs were determined by flow cytometry.

Results: Infected SJL mice with and without anti-IL-10R Ab treatment developed early acute encephalitis and demyelinating leukomyelitis. Immunohistochemistry revealed an increased infiltration of CD3+ T cells in the hippocampus of IL-10R blocked animals at 7 dpi. Moreover, neuronal loss characterized by reduction of NeuN+ cells was found in the pyramidal cell layer associated with an increased number of beta-amyloid precursor protein-expressing axons in the stratum radiatum following receptor blockade. Despite enhanced inflammation in the central nervous system no differences of the viral load were observed between both groups.

Conclusions: IL-10R blockade leads to enhanced virus-induced immunopathology with neuronal loss and axonopathy. Results demonstrate the pivotal role of IL-10 for immune homeostasis and neuroprotection in infectious CNS disorders.