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Chlamydia pneumoniae infection acts as an endothelial stressor with the potential to initiate the earliest heat shock protein 60-dependent inflammatory stage of atherosclerosis

Kreutmayer, Simone ; Csordas, Adam ; Kern, Jan ; Maass, Viola ; Almanzar, Giovanni ; Offterdinger, Martin ; Öllinger, Robert ; Maass, Matthias ; Wick, Georg

In: Cell Stress and Chaperones, 2013, vol. 18, no. 3, p. 259-268

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    Titel
    • Chlamydia pneumoniae infection acts as an endothelial stressor with the potential to initiate the earliest heat shock protein 60-dependent inflammatory stage of atherosclerosis
    Autor
    • Kreutmayer, Simone. Laboratory of Autoimmunity, Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr Strasse 4a, 6020, Innsbruck, Austria
    • Csordas, Adam. Laboratory of Autoimmunity, Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr Strasse 4a, 6020, Innsbruck, Austria
    • Kern, Jan. Institute of Medical Microbiology, Hygiene and Infectious Diseases, Paracelsus Medical Private University of Salzburg, Salzburg, Austria
    • Maass, Viola. Institute of Medical Microbiology, Hygiene and Infectious Diseases, Paracelsus Medical Private University of Salzburg, Salzburg, Austria
    • Almanzar, Giovanni. Laboratory of Autoimmunity, Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr Strasse 4a, 6020, Innsbruck, Austria
    • Offterdinger, Martin. Biooptics Facility, Division of Neurobiochemistry, Biocenter, Innsbruck Medical University, Innsbruck, Austria
    • Öllinger, Robert. Division of Visceral, Transplant and Thorax Surgery, Innsbruck Medical University, Innsbruck, Austria
    • Maass, Matthias. Institute of Medical Microbiology, Hygiene and Infectious Diseases, Paracelsus Medical Private University of Salzburg, Salzburg, Austria
    • Wick, Georg. Laboratory of Autoimmunity, Division of Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr Strasse 4a, 6020, Innsbruck, Austria
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • Cell Stress and Chaperones, 2013, vol. 18, no. 3, p. 259-268. Springer Netherlands
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:313316
    Summary
    We identified increased expression and redistribution of the intracellular protein 60-kDa human heat shock protein (hHSP60) (HSPD1) to the cell surface in human endothelial cells subjected to classical atherosclerosis risk factors and subsequent immunologic cross-reactivity against this highly conserved molecule, as key events occurring early in the process of atherosclerosis. The present study aimed at investigating the role of infectious pathogens as stress factors for vascular endothelial cells and, as such, contributors to early atherosclerotic lesion formation. Using primary donor-matched arterial and venous human endothelial cells, we show that infection with Chlamydia pneumoniae leads to marked upregulation and surface expression of hHSP60 and adhesion molecules. Moreover, we provide evidence for an increased susceptibility of arterial endothelial cells for redistribution of hHSP60 to the cellular membrane in response to C. pneumoniae infection as compared to autologous venous endothelial cells. We also show that oxidative stress has a central role to play in endothelial cell activation in response to chlamydial infection. These data provide evidence for a role of C. pneumoniae as a potent primary endothelial stressor for arterial endothelial cells leading to enrichment of hHSP60 on the cellular membrane and, as such, a potential initiator of atherosclerosis