Bartonella Adhesin A Mediates a Proangiogenic Host Cell Response

Author:

Riess Tanja1,Andersson Siv G.E.2,Lupas Andrei3,Schaller Martin4,Schäfer Andrea1,Kyme Pierre1,Martin Jörg3,Wälzlein Joo-Hee1,Ehehalt Urs1,Lindroos Hillevi2,Schirle Markus5,Nordheim Alfred5,Autenrieth Ingo B.1,Kempf Volkhard A.J.1

Affiliation:

1. Institut für Medizinische Mikrobiologie und Hygiene, Department of Molecular Biology, Eberhard-Karls-Universität, 72076 Tübingen, Germany

2. Department of Molecular Evolution, Evolutionary Biology Center, Uppsala University, 75236 Uppsala, Sweden

3. Max-Planck-Institut für Entwicklungsbiologie, 72076 Tübingen, Germany

4. Universitäts-Hautklinik, Department of Molecular Biology, Eberhard-Karls-Universität, 72076 Tübingen, Germany

5. Institute for Cell Biology, Department of Molecular Biology, Eberhard-Karls-Universität, 72076 Tübingen, Germany

Abstract

Bartonella henselae causes vasculoproliferative disorders in humans. We identified a nonfimbrial adhesin of B. henselae designated as Bartonella adhesin A (BadA). BadA is a 340-kD outer membrane protein encoded by the 9.3-kb badA gene. It has a modular structure and contains domains homologous to the Yersinia enterocolitica nonfimbrial adhesin (Yersinia adhesin A). Expression of BadA was restored in a BadA-deficient transposon mutant by complementation in trans. BadA mediates the binding of B. henselae to extracellular matrix proteins and to endothelial cells, possibly via β1 integrins, but prevents phagocytosis. Expression of BadA is crucial for activation of hypoxia-inducible factor 1 in host cells by B. henselae and secretion of proangiogenic cytokines (e.g., vascular endothelial growth factor). BadA is immunodominant in B. henselae–infected patients and rodents, indicating that it is expressed during Bartonella infections. Our results suggest that BadA, the largest characterized bacterial protein thus far, is a major pathogenicity factor of B. henselae with a potential role in the induction of vasculoproliferative disorders.

Publisher

Rockefeller University Press

Subject

Immunology,Immunology and Allergy

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