Details

Autor(en) / Beteiligte

• Goenka, Radhika
• Parent, Michelle A.
• Elzer, Philip H.
• Baldwin, Cynthia L.

Titel

B Cell-deficient Mice Display Markedly Enhanced Resistance to the Intracellular Bacterium Brucella abortus

Ist Teil von

• The Journal of infectious diseases, 2011-04, Vol.203 (8), p.1136-1146

Ort / Verlag

Oxford: Oxford University Press

Erscheinungsjahr

2011

Quelle

Oxford Journals 2020 Medicine

Beschreibungen/Notizen

• Background. Brucella species are facultative intracellular bacteria that cause lifelong infections in humans and livestock. Methods. Here we evaluated the contribution of B cells in control of murine brucellosis in the more susceptible BALB/c and the more resistant C57BL/6 mice by infecting B cell-deficient mice. Results. Strikingly, in the absence of B cells in both C57BL/6 and BALB/c mice, 99% and 99.5% of the infection found in wild type mice was cleared, respectively. This augmented clearance was not reversed in either strain by passive transfer of immune serum. In C57BL/6 mice, the clearance of infection coincided with an increase in interferon γ (IFN-γ)-producing CD4 and CD8 T cells and a reduction in interleukin 10 (IL-10)-producing cells. In BALB/c mice, this clearance was IFN-γ-dependent, as B cell/IFN-γ dual knockout mice were unable to clear the infection, and was inversely related to the levels of transforming growth factor β (TGF-β). Furthermore, B cells were found to produce TGF-β and IL-10 during early stages of infection in BALB/c wild-type and C57BL/6 wild-type mice, respectively. Conclusions. Thus, we demonstrate that the establishment of the high plateau phase of infection is dependent on non-antibody-mediated B cell effector mechanisms, including B regulatory functions, during murine brucellosis.