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Infection and Immunity, July 2008, p. 3207-3213, Vol. 76, No. 7
0019-9567/08/$08.00+0     doi:10.1128/IAI.00203-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Inactivation of the Type IV Secretion System Reduces the Th1 Polarization of the Immune Response to Brucella abortus Infection{triangledown}

Hortensia García Rolán1,2 and Renée M. Tsolis1,2*

Department of Medical Microbiology and Immunology, University of California at Davis, One Shields Avenue, Davis, California 95616,1 Department of Medical Microbiology and Immunology, Texas A&M University System Health Science Center, College Station, Texas 77843-11142

Received 13 February 2008/ Returned for modification 3 April 2008/ Accepted 25 April 2008

The Brucella abortus type IV secretion system (T4SS), encoded by the virB operon, is essential for establishing persistent infection in the murine reticuloendothelial system. To gain insight into the in vivo interactions mediated by the T4SS, we compared host responses elicited by B. abortus with those of an isogenic mutant in the virB operon. Mice infected with the B. abortus virB mutant elicited smaller increases in serum levels of immunoglobulin G2a, gamma interferon (IFN-{gamma}), and interleukin-12p40 than did mice infected with wild-type B. abortus. Despite equal bacterial loads in the spleen, at 3 to 4 days postinfection, levels of IFN-{gamma} were higher in mice infected with wild-type B. abortus than in mice infected with the virB mutant, as shown by real-time PCR, intracellular cytokine staining, and cytokine levels. IFN-{gamma}-producing CD4+ T cells were more abundant in spleens of mice infected with wild-type B. abortus than in virB mutant-infected mice. Similar numbers of IFN-{gamma}-secreting CD8+ T cells were observed in the spleens of mice infected with B. abortus 2308 or a virB mutant. These results suggest that early differences in cytokine responses contribute to a stronger Th1 polarization of the immune response in mice infected with wild-type B. abortus than in mice infected with the virB mutant.

* 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) 754-7420. E-mail: rmtsolis{at}ucdavis.edu

{triangledown} Published ahead of print on 5 May 2008.

Editor: J. B. Bliska

Infection and Immunity, July 2008, p. 3207-3213, Vol. 76, No. 7
0019-9567/08/$08.00+0     doi:10.1128/IAI.00203-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Rolan, H. G., Xavier, M. N., Santos, R. L., Tsolis, R. M. (2009). Natural Antibody Contributes to Host Defense against an Attenuated Brucella abortus virB Mutant. Infect. Immun. 77: 3004-3013 [Abstract] [Full Text]  


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