The putative iron transport system SitABCD encoded on SPI1 is required for full virulence of Salmonella typhimurium

被引:176
作者
Janakiraman, A [1 ]
Slauch, JM [1 ]
机构
[1] Univ Illinois, Dept Microbiol, Urbana, IL 61801 USA
关键词
D O I
10.1046/j.1365-2958.2000.01783.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Salmonella typhimurium is an invasive pathogen that causes diseases ranging from mild gastroenteritis to enteric fever. During the infection process, S. typhimurium induces a number of virulence genes required to circumvent host defences and/or acquire nutrients in the host. We have used the in vivo expression technology (IVET) system to select for S. typhimurium genes that are induced after invasion of a murine cultured cell line. We have characterized a putative iron transporter in Salmonella pathogenicity island 1, termed sitABCD. The sitABCD operon is induced under iron-deficient conditions in vitro and is repressed by Fur. This locus is induced in the animal specifically after invasion of the intestinal epithelium. We show that a sit null mutant is significantly attenuated in BALB/c mice, suggesting that SitABCD plays an important role in iron acquisition in the animal.
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页码:1146 / 1155
页数:10
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