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Infection and Immunity, August 2001, p. 5088-5097, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.5088-5097.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Bartonella henselae Induces NF-kappa B-Dependent Upregulation of Adhesion Molecules in Cultured Human Endothelial Cells: Possible Role of Outer Membrane Proteins as Pathogenic Factors

Oliver Fuhrmann,1 Mardjan Arvand,2 Alexander Göhler,1 Michael Schmid,3 Matthias Krüll,1 Stefan Hippenstiel,1 Joachim Seybold,1 Christoph Dehio,3 and Norbert Suttorp1,*

Department of Internal Medicine (Infectious Diseases), Charité, Humboldt-University of Berlin, 13353 Berlin,1 and Institute of Infectious Diseases, University Hospital Benjamin Franklin, Free University of Berlin, 12203 Berlin,2 Germany, and Division of Molecular Microbiology, Biozentrum of the University of Basel, CH-4056 Basel, Switzerland3

Received 13 September 2000/Returned for modification 20 November 2000/Accepted 4 May 2001

The endothelium is a specific target for Bartonella henselae, and endothelial cell infection represents an important step in the pathogenesis of cat scratch disease and bacillary angiomatosis. Mechanisms of Bartonella-endothelial cell interaction as well as signaling pathways involved in target cell activation were analyzed. B. henselae strain Berlin-1, isolated from bacillary angiomatosis lesions of a human immunodeficiency virus-infected patient, potently stimulated human umbilical cord vein endothelial cells (HUVEC), as determined by NF-kappa B activation and enhanced adhesion molecule expression. These effects were accompanied by increased PMN rolling on and adhesion to infected endothelial cell monolayers, as measured in a parallel-plate flow chamber assay. Monoclonal antibodies against E-selectin significantly reduced PMN rolling and adhesion. In our hands, B. henselae Berlin-1 was substantially more active than the typing strain B. henselae ATCC 49882. E-selectin and ICAM-1 upregulation occurred for up to 9 days, as verified by Northern blotting and cell surface enzyme-linked immunosorbent assay. Induction of adhesion molecules was mediated via NF-kappa B activation and could be blocked by a specific NF-kappa B inhibitor. Additional studies indicated that B. henselae-induced effects did not require living bacteria or Bartonella lipopolysaccharides. Exposure of HUVEC to purified B. henselae outer membrane proteins (OMPs), however, reproduced all aspects of endothelial cell activation. In conclusion, B. henselae, the causative agent of cat scratch disease and bacillary angiomatosis, infects and activates endothelial cells. B. henselae OMPs are sufficient to induce NF-kappa B activation and adhesion molecule expression followed by enhanced rolling and adhesion of leukocytes. These observations identify important new properties of B. henselae, demonstrating its capacity to initiate a cascade of events culminating in a proinflammatory phenotype of infected endothelial cells.

* Corresponding author. Mailing address: Medizinische Klinik m.S. Infektiologie, Charité, Campus Virchow-Klinikum, Humboldt-Universität, Augustenburger Platz 1, 13353 Berlin, Germany. Phone: 49-30-450-553051. Fax: 49-30-450-553906. E-mail: norbert.suttorp{at}charite.de.

Infection and Immunity, August 2001, p. 5088-5097, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.5088-5097.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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