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lpf菌毛操纵子介导鼠伤寒沙门氏菌与小鼠派伊尔结的黏附。

The lpf fimbrial operon mediates adhesion of Salmonella typhimurium to murine Peyer's patches.

作者信息

Bäumler A J, Tsolis R M, Heffron F

机构信息

Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland 97201-3098, USA.

出版信息

Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):279-83. doi: 10.1073/pnas.93.1.279.

Abstract

We investigated the role of the Salmonella typhimurium fimbrial operon formed by the genes lpfABCDE in infection of mice. A mutant in lpfC, the gene encoding the fimbrial outer membrane usher, had an approximately 5-fold increased 50% lethal dose when administered orally to mice. When mice were infected with a mixture of the lpfC mutant and isogenic wild-type S. typhimurium, the lpfC mutant was recovered in lower numbers from Peyer's patches, mesenteric lymph nodes, liver, and spleen. In an organ culture model using murine intestinal loops, lpfC mutants were shown to be associated in lower numbers than wild-type bacteria with Peyer's patches but not with villous intestine. The defect of the lpfC mutant in adhesion to Peyer's patches could be complemented by introducing lpfABCDE on a cosmid. Similarly, heterologous expression of the Salmonella lpf operon in Escherichia coli resulted in an increased adhesion to histological thin sections of Peyer's patch lymph follicles. Electron microscopic analysis of histological sections taken from Peyer's patches after intragastric infection of mice showed that, in contrast to the S. typhimurium wild type, the isogenic lpfC mutant did not destroy M cells of the follicle-associated epithelium. These data show that the Salmonella lpf operon is involved in adhesion to murine Peyer's patches.

摘要

我们研究了由lpfABCDE基因构成的鼠伤寒沙门氏菌菌毛操纵子在小鼠感染中的作用。lpfC基因编码菌毛外膜组装分子,该基因的突变体经口服给予小鼠时,其半数致死剂量增加了约5倍。当用lpfC突变体和同基因野生型鼠伤寒沙门氏菌的混合物感染小鼠时,从派伊尔结、肠系膜淋巴结、肝脏和脾脏中回收的lpfC突变体数量较少。在使用小鼠肠袢的器官培养模型中,与野生型细菌相比,lpfC突变体与派伊尔结的结合数量较少,但与绒毛肠无此现象。通过在黏粒上引入lpfABCDE,可以弥补lpfC突变体在黏附派伊尔结方面的缺陷。同样,沙门氏菌lpf操纵子在大肠杆菌中的异源表达导致其对派伊尔结淋巴滤泡组织学薄片的黏附增加。对小鼠胃内感染后取自派伊尔结的组织切片进行电子显微镜分析表明,与鼠伤寒沙门氏菌野生型不同,同基因lpfC突变体不会破坏滤泡相关上皮的M细胞。这些数据表明,沙门氏菌lpf操纵子参与了对小鼠派伊尔结的黏附。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/498a/40222/d0c5cb122136/pnas01505-0291-a.jpg

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