Plasmacytoid Dendritic Cells Are Crucial in Bifidobacterium adolescentis-Mediated Inhibition of Yersinia enterocolitica Infection

Plasmacytoid Dendritic Cells Are Crucial in Bifidobacterium adolescentis-Mediated Inhibition of Yersinia enterocolitica Infection
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浆细胞样树突状细胞在青春双歧杆菌介导的小肠结肠炎耶尔森氏菌感染抑制中至关重要

DOI:
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
J. Frick
J. Frick
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Alexandra Wittmann;I. Autenrieth;J. Frick

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在工业化国家,细菌性肠道感染通常是由致病性肠杆菌科引起的。微生物群与宿主免疫系统的相互作用决定了对病原体的适当反应的充分性。在这项研究中,我们探讨了益生菌青少年双歧杆菌是否在肠道结肠炎耶尔森菌感染期间具有保护作用。雌性C57BL/6小鼠分别饲喂感染小肠结肠炎耶尔森菌的青春期贝氏杆菌,或饲喂后感染小肠结肠炎耶尔森菌的青春期贝氏杆菌。与感染耶尔森氏菌的小鼠相比,喂食感染耶尔森氏菌的小鼠和喂养感染耶尔森氏菌的小鼠的青少年可以免受耶尔森氏菌感染,这表明体重减轻和脾脏耶尔森氏菌负荷显著减少。此外,对感染的保护与肠道浆细胞样树突状细胞和调节性t细胞频率的增加有关。通过消耗实验研究了浆细胞样树突状细胞的功能,通过注射抗小鼠PDCA-1抗体来消耗耶尔森菌感染的C57BL/6小鼠,或各自的同型对照。浆细胞样树突状细胞耗竭后,青春期芽孢杆菌介导的防止耶尔森氏菌传播到脾脏的保护作用被取消,这表明pDC在控制肠道耶尔森氏菌感染方面具有重要作用。我们认为,从浆细胞样树突状细胞和调节性t细胞频率增加的角度来说,喂养青春期芽孢杆菌调节了肠道免疫系统,这可能解释了青春期芽孢杆菌介导的对小肠结肠炎耶尔森菌感染的保护作用。
In industrialized countries bacterial intestinal infections are commonly caused by enteropathogenic Enterobacteriaceae. The interaction of the microbiota with the host immune system determines the adequacy of an appropriate response against pathogens. In this study we addressed whether the probiotic Bifidobacterium adolescentis is protective during intestinal Yersinia enterocolitica infection. Female C57BL/6 mice were fed with B. adolescentis, infected with Yersinia enterocolitica, or B. adolescentis fed and subsequently infected with Yersinia enterocolitica. B. adolescentis fed and Yersinia infected mice were protected from Yersinia infection as indicated by a significantly reduced weight loss and splenic Yersinia load when compared to Yersinia infected mice. Moreover, protection from infection was associated with increased intestinal plasmacytoid dendritic cell and regulatory T-cell frequencies. Plasmacytoid dendritic cell function was investigated using depletion experiments by injecting B. adolescentis fed, Yersinia infected C57BL/6 mice with anti-mouse PDCA-1 antibody, to deplete plasmacytoid dendritic cells, or respective isotype control. The B. adolescentis-mediated protection from Yersinia dissemination to the spleen was abrogated after plasmacytoid dendritic cell depletion indicating a crucial function for pDC in control of intestinal Yersinia infection. We suggest that feeding of B. adolescentis modulates the intestinal immune system in terms of increased plasmacytoid dendritic cell and regulatory T-cell frequencies, which might account for the B. adolescentis-mediated protection from Yersinia enterocolitica infection.
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