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Infection and Immunity, July 2009, p. 3004-3013, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.01114-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Natural Antibody Contributes to Host Defense against an Attenuated Brucella abortus virB Mutant{triangledown}

Hortensia G. Rolán,1 Mariana N. Xavier,2 Renato L. Santos,2 and Renée M. Tsolis1*

Department of Medical Microbiology and Immunology, University of California, One Shields Avenue, Davis, California 95616,1 Departamento de Clínica e Cirurgia Veterinária, Escola de Veterinária, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, 31270-901 Belo Horizonte, MG, Brazil2

Received 5 September 2008/ Returned for modification 22 October 2008/ Accepted 29 March 2009

Brucella abortus is an intracellular pathogen that persists within phagocytic cells of the reticuloendothelial system. To identify in vivo interactions between B. abortus and the host that lead to persistent infection, we studied the persistence of B. abortus and an isogenic virB mutant deficient in the VirB type IV secretion system (T4SS) in knockout mice. In contrast to control mice, mice lacking B cells (Igh6–/–) were permissive for infection with the attenuated virB mutant. To determine the basis for this phenotype, we characterized immune functions of Igh6–/– mice in the context of B. abortus infection. Igh6–/– mice had greater numbers of extracellular bacteria in the spleen and increased early expression of proinflammatory cytokines during B. abortus infection. Further, a virB mutant, despite its wild-type level of survival, failed to elicit microgranuloma formation in the spleens of Igh6–/– mice, suggesting a requirement for the T4SS to elicit this pathological change. Passive transfer of immunoglobulin G from naïve mice restored the ability of Igh6–/– mice to control the persistence of the virB mutant by a complement-independent mechanism. Further, adoptive transfer of CD11b+ cells from C57BL/6 mice to Igh6–/– mice restored the ability of the knockout mice to limit the replication of the virB mutant in the spleen, suggesting that the Igh6–/– mutation affects phagocyte function and that phagocyte function can be restored by natural antibody.

* Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, University of California, One Shields Avenue, Davis, CA 95616. Phone: (530) 754-8497. Fax: (530) 754-7240. E-mail: rmtsolis{at}ucdavis.edu

{triangledown} Published ahead of print on 13 April 2009.

Editor: J. B. Bliska

Infection and Immunity, July 2009, p. 3004-3013, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.01114-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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