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Bacterial Colitis Increases Susceptibility to Oral Prion Disease

Sigurdson, Christina J. ; Heikenwalder, Mathias ; Manco, Giuseppe ; Barthel, Manja ; Schwarz, Petra ; Stecher, Bärbel ; Krautler, Nike J. ; Hardt, Wolf-Dietrich ; Seifert, Burkhardt ; MacPherson, Andrew J. S. ; Corthesy, Irène ; Aguzzi, Adriano

In: The Journal of Infectious Diseases, 2009, vol. 199, no. 2, p. 243-252

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    Titel
    • Bacterial Colitis Increases Susceptibility to Oral Prion Disease
    Autor
    • Sigurdson, Christina J.. Institutes of Neuropathology, University Hospital of Zürich
    • Heikenwalder, Mathias. Institutes of Neuropathology, University Hospital of Zürich
    • Manco, Giuseppe. Institutes of Neuropathology, University Hospital of Zürich
    • Barthel, Manja. Institute of Microbiology, Eidgenössische Technische Hochschule Zürich, University of Zürich, Zürich
    • Schwarz, Petra. Institutes of Neuropathology, University Hospital of Zürich
    • Stecher, Bärbel. Institute of Microbiology, Eidgenössische Technische Hochschule Zürich, University of Zürich, Zürich
    • Krautler, Nike J.. Institutes of Neuropathology, University Hospital of Zürich
    • Hardt, Wolf-Dietrich. Institute of Microbiology, Eidgenössische Technische Hochschule Zürich, University of Zürich, Zürich
    • Seifert, Burkhardt. Biostatistics Unit, Institute of Social and Preventive Medicine, University of Zürich, Zürich
    • MacPherson, Andrew J. S.. Institutes of Experimental Immunology, University Hospital of Zürich
    • Corthesy, Irène. Nestlé Research Center, Lausanne, Switzerland
    • Aguzzi, Adriano. Institutes of Neuropathology, University Hospital of Zürich
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • The Journal of Infectious Diseases, 2009, vol. 199, no. 2, p. 243-252. The University of Chicago Press
    Andere elektronische Ausgabe
    Klassifikation
    • Gesundheit
    OAI-PMH-ID
    • oai:doc.rero.ch:298239
    Summary
    Dietary exposure to prion-contaminated materials has caused kuru and variant Creutzfeldt-Jakob disease in humans and transmissible spongiform encephalopathies (TSEs) in cattle, mink, and felines. The epidemiology of dietary prion infections suggests that host genetic modifiers and possibly exogenous cofactors may play a decisive role in determining disease susceptibility. However, few cofactors influencing susceptibility to prion infection have been identified. In the present study,we investigated whether colitis might represent one such cofactor.Were port that moderate colitis caused by an attenuated Salmonella strain more than doubles the susceptibility of mice to oral prion infection and modestly accelerates the development of disease after prion challenge. The prion protein was up-regulated in intestines and mesenteric lymph nodes of mice with colitis, providing a possible mechanism for the effect of colitis on the pathogenesis of prion disease. Therefore, moderate intestinal inflammation at the time of prion exposure may constitute one of the elusive risk factors underlying the development of TSE