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Infection and Immunity, January 2007, p. 35-43, Vol. 75, No. 1
0019-9567/07/$08.00+0     doi:10.1128/IAI.00963-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Analysis of Bartonella Adhesin A Expression Reveals Differences between Various B. henselae Strains{triangledown} ,{dagger}

Tanja Riess,1 Günter Raddatz,2 Dirk Linke,3 Andrea Schäfer,1 and Volkhard A. J. Kempf1*

Institut für Medizinische Mikrobiologie und Hygiene, Eberhard-Karls-Universität, Elfriede-Aulhorn-Str. 6, 72076 Tübingen, Germany,1 Max-Planck-Institut für biologische Kybernetik, Spemannstr. 34, 72076 Tübingen, Germany,2 Max-Planck-Institut für Entwicklungsbiologie, Abteilung Proteinevolution, Spemannstr. 35, 72076 Tübingen, Germany3

Received 16 June 2006/ Returned for modification 16 August 2006/ Accepted 6 October 2006

Bartonella henselae causes cat scratch disease and the vasculoproliferative disorders bacillary angiomatosis and peliosis hepatis in humans. One of the best known pathogenicity factors of B. henselae is Bartonella adhesin A (BadA), which is modularly constructed, consisting of head, neck/stalk, and membrane anchor domains. BadA is important for the adhesion of B. henselae to extracellular-matrix proteins and endothelial cells (ECs). In this study, we analyzed different B. henselae strains for BadA expression, autoagglutination, fibronectin (Fn) binding, and adhesion to ECs. We found that the B. henselae strains Marseille, ATCC 49882, Freiburg 96BK3 (FR96BK3), FR96BK38, and G-5436 express BadA. Remarkably, BadA expression was lacking in a B. henselae ATCC 49882 variant, in strains ATCC 49793 and Berlin-1, and in the majority of bacteria of strain Berlin-2. Adherence of B. henselae to ECs and Fn reliably correlated with BadA expression. badA was present in all tested strains, although the length of the gene varied significantly due to length variations of the stalk region. Sequencing of the promoter, head, and membrane anchor regions revealed only minor differences that did not correlate with BadA expression, apart from strain Berlin-1, in which a 1-bp deletion led to a frameshift in the head region of BadA. Our data suggest that, apart from the identified genetic modifications (frameshift deletion and recombination), other so-far-unknown regulatory mechanisms influence BadA expression. Because of variations between and within different B. henselae isolates, BadA expression should be analyzed before performing infection experiments with B. henselae.

* Corresponding author. Mailing address: Institut für Medizinische Mikrobiologie und Hygiene, Elfriede-Aulhorn-Str. 6, D-72076 Tübingen, Germany. Phone: 49-7071-2981526. Fax: 49-7071-295440. E-mail: volkhard.kempf{at}med.uni-tuebingen.de.

{triangledown} Published ahead of print on 23 October 2006.

Editor: J. L. Flynn

{dagger} Supplemental material for this article may be found at http://iai.asm.org/.

Infection and Immunity, January 2007, p. 35-43, Vol. 75, No. 1
0019-9567/07/$08.00+0     doi:10.1128/IAI.00963-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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