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Infection and Immunity, January 2008, p. 250-262, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.00949-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Brucella abortus Inhibits Major Histocompatibility Complex Class II Expression and Antigen Processing through Interleukin-6 Secretion via Toll-Like Receptor 2{triangledown}

Paula Barrionuevo,1,2 Juliana Cassataro,1,2 M. Victoria Delpino,1 Astrid Zwerdling,1,2 Karina A. Pasquevich,1,2 Clara García Samartino,1,2 Jorge C. Wallach,3 Carlos A. Fossati,1 and Guillermo H. Giambartolomei1,2*

Instituto de Estudios de la Inmunidad Humoral (CONICET), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina,1 Laboratorio de Inmunogenética, Hospital de Clínicas "José de San Martín," Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina,2 Sección Brucelosis, Hospital F. J. Muñiz, Buenos Aires, Argentina3

Received 12 July 2007/ Returned for modification 21 August 2007/ Accepted 12 October 2007

The strategies that allow Brucella abortus to survive inside macrophages for prolonged periods and to avoid the immunological surveillance of major histocompatibility complex class II (MHC-II)-restricted gamma interferon (IFN-{gamma})-producing CD4+ T lymphocytes are poorly understood. We report here that infection of THP-1 cells with B. abortus inhibited expression of MHC-II molecules and antigen (Ag) processing. Heat-killed B. abortus (HKBA) also induced both these phenomena, indicating the independence of bacterial viability and involvement of a structural component of the bacterium. Accordingly, outer membrane protein 19 (Omp19), a prototypical B. abortus lipoprotein, inhibited both MHC-II expression and Ag processing to the same extent as HKBA. Moreover, a synthetic lipohexapeptide that mimics the structure of the protein lipid moiety also inhibited MHC-II expression, indicating that any Brucella lipoprotein could down-modulate MHC-II expression and Ag processing. Inhibition of MHC-II expression and Ag processing by either HKBA or lipidated Omp19 (L-Omp19) depended on Toll-like receptor 2 and was mediated by interleukin-6. HKBA or L-Omp19 also inhibited MHC-II expression and Ag processing of human monocytes. In addition, exposure to the synthetic lipohexapeptide inhibited Ag-specific T-cell proliferation and IFN-{gamma} production of peripheral blood mononuclear cells from Brucella-infected patients. Together, these results indicate that there is a mechanism by which B. abortus may prevent recognition by T cells to evade host immunity and establish a chronic infection.

* Corresponding author. Mailing address: Instituto de Estudios de la Inmunidad Humoral (IDEHU), Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Junín 956 4° Piso, 1113 Buenos Aires, Argentina. Phone: 54 11 5950-8755. Fax: 54 11 5950-8758. E-mail: ggiambart{at}ffyb.uba.ar

{triangledown} Published ahead of print on 5 November 2007.

Editor: R. P. Morrison

Infection and Immunity, January 2008, p. 250-262, Vol. 76, No. 1
0019-9567/08/$08.00+0     doi:10.1128/IAI.00949-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wilson, J. E., Katkere, B., Drake, J. R. (2009). Francisella tularensis Induces Ubiquitin-Dependent Major Histocompatibility Complex Class II Degradation in Activated Macrophages. Infect. Immun. 77: 4953-4965 [Abstract] [Full Text]  


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