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前沿:流产布鲁氏菌利用肠道 M 细胞上的细胞朊病毒蛋白作为入侵受体。

Cutting Edge: Brucella abortus exploits a cellular prion protein on intestinal M cells as an invasive receptor.

机构信息

Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, Kanagawa 230-0045, Japan;

出版信息

J Immunol. 2012 Aug 15;189(4):1540-4. doi: 10.4049/jimmunol.1103332. Epub 2012 Jul 6.

Abstract

Brucella abortus is a Gram-negative bacterium causing brucellosis. Although B. abortus is known to infect via the oral route, the entry site in the gastrointestinal tract has been unclear. We found that B. abortus was selectively internalized by microfold cells (M cells), a subset of epithelial cells specialized for mucosal Ag uptake. During this process, colocalization of cellular prion protein (PrP(C)) and B. abortus was evident on the apical surface as well as in subapical vacuolar structures in M cells. Internalization of B. abortus by M cells of PrP(C)-deficient (Prnp(-/-)) mice was greatly reduced compared with that in wild-type mice. Furthermore, an oral infection study revealed that translocation of B. abortus into the Peyer's patch was significantly lower in Prnp(-/-) than in wild-type mice. These observations suggest that orally infected B. abortus invades the host through M cells by using PrP(C) on the apical surface of M cells as an uptake receptor.

摘要

流产布鲁氏菌是一种革兰氏阴性细菌,可引起布鲁氏菌病。虽然已知流产布鲁氏菌通过口服途径感染,但胃肠道的进入部位尚不清楚。我们发现流产布鲁氏菌被微褶细胞(M 细胞)选择性内化,M 细胞是专门用于黏膜 Ag 摄取的上皮细胞的一个亚群。在此过程中,细胞朊蛋白(PrP(C))和流产布鲁氏菌在 M 细胞的顶端表面以及亚顶端空泡结构中明显共定位。与野生型小鼠相比,缺乏细胞朊蛋白(Prnp(-/-))的小鼠 M 细胞内化流产布鲁氏菌的能力大大降低。此外,一项口服感染研究表明,Prnp(-/-)小鼠向派尔集合淋巴结的流产布鲁氏菌易位明显低于野生型小鼠。这些观察结果表明,通过 M 细胞顶端表面上的 PrP(C)作为摄取受体,口服感染的流产布鲁氏菌通过 M 细胞入侵宿主。

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