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B 细胞缺陷小鼠对细胞内细菌布鲁氏菌表现出明显增强的抵抗力。

B cell-deficient mice display markedly enhanced resistance to the intracellular bacterium Brucella abortus.

机构信息

University of Massachusetts, Amherst, MA 01003, USA.

出版信息

J Infect Dis. 2011 Apr 15;203(8):1136-46. doi: 10.1093/infdis/jiq171.

DOI:10.1093/infdis/jiq171
PMID:21451002
Abstract

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.

摘要

背景

布鲁氏菌属是兼性细胞内细菌,可在人类和牲畜中引起终身感染。

方法

在这里,我们通过感染 B 细胞缺陷型小鼠来评估 B 细胞在控制更易感的 BALB/c 和更具抗性的 C57BL/6 小鼠中的鼠布鲁氏菌病中的作用。

结果

令人惊讶的是,在 C57BL/6 和 BALB/c 小鼠中没有 B 细胞的情况下,分别清除了野生型小鼠中发现的感染的 99%和 99.5%。在这两种菌株中,通过被动转移免疫血清均未逆转这种增强的清除作用。在 C57BL/6 小鼠中,感染的清除与干扰素 γ (IFN-γ) 产生的 CD4 和 CD8 T 细胞的增加以及白细胞介素 10 (IL-10) 产生细胞的减少相吻合。在 BALB/c 小鼠中,这种清除作用是 IFN-γ 依赖性的,因为 B 细胞/IFN-γ 双重敲除小鼠无法清除感染,并且与转化生长因子 β (TGF-β) 的水平呈负相关。此外,在 BALB/c 野生型和 C57BL/6 野生型小鼠中,分别在感染的早期阶段发现 B 细胞产生 TGF-β 和 IL-10。

结论

因此,我们证明在鼠布鲁氏菌病中,高平台阶段感染的建立依赖于非抗体介导的 B 细胞效应机制,包括 B 调节功能。

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