gms | German Medical Science

60. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

26. - 28.08.2015, Berlin

Role of Lipocalin 2 in virally induced neuroinflammatory processes by the use of BDV-infected TNF-transgenic and TNF receptor k.o.-mice

Meeting Abstract

  • corresponding author Julia Vienenkoetter - Institut für Veterinär-Pathologie JLU Gießen, Gießen, Germany
  • Ulrich L. M. Eisel - Faculty of Mathematics and Natural Sciences, Molecular Neurobiology — Groningen Institute for Evolutionary Life Sciences, Groningen, Netherlands
  • Carsten Culmsee - Institut für Pharmakologie und Klinische Pharmazie Philipps-Universität Marburg, Marburg, Germany
  • Manuela Hirz - Institut für Veterinär-Pathologie JLU Gießen, Gießen, Germany
  • presenting/speaker Christiane Herden - Institut für Veterinär-Pathologie JLU Gießen, Gießen, 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. Doc15dgnnP27

doi: 10.3205/15dgnn51, urn:nbn:de:0183-15dgnn512

Veröffentlicht: 25. August 2015

© 2015 Vienenkoetter et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe



Objective:Lipocalin 2 (Lcn 2) acts as a cytokine involved in the regulation of neuroinflammatory processes. It is supposed to promote classical proinflammatory activation of astrocytes and microglia via a TNFα- and NFκB-dependent TNFR1 mediated pathway [1], [2]. It has been shown that the neurotropic Borna disease virus (BDV) has an inhibitory effect on the activation of the transcription factor NFκB in order to evade an effective antiviral immune response [3]. Here, Lcn 2 expression under neuroinflammatory conditions was investigated with particular focus on possible interferences between BDV-infection and the TNF-status.

Materials and methods: FFPE brain tissue was obtained from BDV-infected or non-infected wildtype (wt)- and mice with a neuronal TNF overexpression (TNFtg) in cerebral cortex, striatum, thalamus and hippocampus as well as TNFR1- and TNFR2-k.o. mice which were euthanized 21, 42 or 49 dpi. Lcn 2 expression was examined in sections with TNF overexpression and the cerebellum. Cellular origin of Lcn 2 was further determined by double-labelling with anti-GFAP and -Iba1 antibodies.

Results: BDV-infected TNFtg mice exhibited strong intracytoplasmic staining predominantly in astrocytes with a strong hypertrophy and to a lesser extent in activated microglia (as well as a diffuse parenchymal signal) at 42 and 49 dpi. Interestingly, certain brain areas, particularly the striatum, showed strong Lcn 2 expression in comparison to others. BDV-infected wt and TNFR1-k.o. and TNFR2-k.o. mice did not show any detectable Lcn 2 signals as well as non-infected control mice. In a group of BDV-infected TNFR1-k.o. and TNFR2-k.o. mice with epileptic seizures rare Lcn 2-positive cells were found.

Conclusion: Lcn 2 expression can be induced by increased TNF levels and neurotropic virus infection being associated with an unusual astrocytic hypertrophy and microglial activation. The reason for the Lcn 2 expression predominantly in the striatum has to be assessed in further studies.


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