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Infection and Immunity, October 2005, p. 6782-6790, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6782-6790.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Analysis of the Behavior of eryC Mutants of Brucella suis Attenuated in Macrophages

Sonja Burkhardt,1 Maria P. Jiménez de Bagüés,2 Jean-Pierre Liautard,1 and Stephan Köhler1*

Institut National de la Santé et de la Recherche Médicale U-431, Université Montpellier II, 34095 Montpellier, France,1 Unidad de Sanidad Animal, Centro de Investigación y Tecnología Agroalimentaria, Gobierno de Aragón, Ap. 727, 50080 Zaragoza, Spain2

Received 30 March 2005/ Returned for modification 2 May 2005/ Accepted 3 June 2005

The facultatively intracellular pathogen Brucella, characterized by its capacity to replicate in professional and non professional phagocytes, also causes abortion in ruminants. This property has been linked to the presence of erythritol in the placenta, as brucellae preferentially utilize erythritol. The ery operon encodes enzymes involved in erythritol metabolism, and a link with virulence has since been discussed. Allelic exchange mutants in eryC of Brucella suis were erythritol sensitive in vitro with a MIC of 1 to 5 mM of erythritol. Their multiplication in macrophage-like cells was 50- to 90-fold reduced, but complementation of the mutant restored wild-type levels of intracellular multiplication and the capacity to use erythritol as a sole carbon source. In vivo, the eryC mutant colonized the spleens of infected BALB/c mice to a significantly lower extent than the wild type and the complemented strain. Interestingly, eryC mutants that were in addition spontaneously erythritol tolerant nevertheless exhibited wild-type-like intramacrophagic and intramurine replication. We concluded from our results that erythritol was not an essential carbon source for the pathogen in the macrophage host cell but that the inactivation of the eryC gene significantly reduced the intramacrophagic and intramurine fitness of B. suis.


* Corresponding author. Mailing address: INSERM U-431, Université Montpellier II, C.P. 100, Pl. E. Bataillon, 34095 Montpellier, France. Phone: (33) 4 67 14 42 38. Fax: (33) 4 67 14 33 38. E-mail: kohler{at}univ-montp2.fr.

Editor: D. L. Burns


Infection and Immunity, October 2005, p. 6782-6790, Vol. 73, No. 10
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.10.6782-6790.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.







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