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This article is part of the supplement: Infectious diseases of the nervous system: pathogenesis and worldwide impact

Open Access Oral presentation

Astrocyte gp130-expression is critical for the control of Toxoplasma encephalitis

Katrin Drögemüller1, Ulrike Helmuth1, Anna Brunn2, Monika Sakowicz-Burkiewicz12, Dirk Reinhold3, David H Gutmann4, Werner Mueller56, Martina Deckert2 and Dirk Schlüter1*

Author Affiliations

1 Institut für Medizinische Mikrobiologie, OvG Universität Magdeburg, 39120 Magdeburg, Germany

2 Abteilung für Neuropathologie, Universität zu Köln, 50937 Köln, Germany

3 Institut für Immunologie, OvG Universität Magdeburg, 39120 Magdeburg, Germany

4 Department of Neurology, Washington University School of Medicine, St. Louis, MO 63110, USA

5 Helmholtz-Zentrum für Infektionsforschung, 38124 Braunschweig, Germany

6 University of Manchester, Manchester, UK

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BMC Proceedings 2008, 2(Suppl 1):S10  doi:

The electronic version of this article is the complete one and can be found online at:

Published:23 September 2008

© 2008 Drögemüller et al; licensee BioMed Central Ltd.

Oral presentation

Toxoplasma (T.) gondii infects astrocytes, neurons and microglia cells in the CNS and, after acute encephalitis, persists within neurons. Robust astrocyte activation is a hallmark of Toxoplasma encephalitis (TE); however, the in vivo function of astrocytes is largely unknown. To study their role in TE, we generated C57BL/6 GFAP-Cre gp130fl/fl mice, which lack gp130, the signal transducing receptor for IL-6 family cytokines, in their astrocytes. In TE of wildtype mice, the gp130 ligands IL-6, IL-11, IL-27, LIF, oncostatin M, ciliary neurotrophic factor, B cell stimulating factor, and cardiotrophin-1 were upregulated. In addition, GFAP+ astrocytes of gp130fl/fl control mice were activated, increased in number, and efficiently restricted inflammatory lesions and parasites, thereby, contributing to survival from TE. In contrast, T. gondii-infected GFAP-Cre gp130fl/fl mice lost GFAP+ astrocytes in inflammatory lesions resulting in an inefficient containment of inflammatory lesions, impaired parasite control and, ultimately, a lethal necrotizing TE. Production of IFN-gamma and IGTP, which mediate parasite control in astrocytes, were even increased in GFAP-Cre gp130fl/fl mice indicating that instead of the direct anti-parasitic effect the immunoregulatory function of GFAP-Cre gp130fl/fl astrocytes was disturbed. Correspondingly, in vitro infected GFAP-Cre gp130fl/fl astrocytes inhibited growth of T. gondii efficiently after stimulation with IFN-gamma, whereas neighbouring non-infected and TNF-stimulated GFAP-Cre gp130fl/fl astrocytes became apoptotic. Collectively, these are the first experiments demonstrating a crucial function of astrocytes in CNS infection.