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大肠杆菌K-12亚铁摄取突变体在定殖于小鼠肠道的能力方面存在缺陷。

Escherichia coli K-12 ferrous iron uptake mutants are impaired in their ability to colonize the mouse intestine.

作者信息

Stojiljkovic I, Cobeljic M, Hantke K

机构信息

Mikrobiologie II, Tübingen, FRG, Institute for Preventive Medicine, Beograd, Crnotravska, Yugoslavia.

出版信息

FEMS Microbiol Lett. 1993 Mar 15;108(1):111-5. doi: 10.1111/j.1574-6968.1993.tb06082.x.

DOI:10.1111/j.1574-6968.1993.tb06082.x
PMID:8472918
Abstract

The streptomycin-treated mouse colonization model was used to investigate the role of the Fe2+ uptake system (Feo) of Escherichia coli K12 in the colonization of the mouse intestine. Mutants impaired in the uptake of Fe2+ ions were shown to be deficient also in their colonization ability. Both enterochelin-producing and enterochelin-nonproducing Escherichia coli feo mutants were unable to colonize the mouse intestine. These results demonstrated that Fe(II) is an essential source of iron for E. coli grown in the intestine.

摘要

采用链霉素处理的小鼠定殖模型来研究大肠杆菌K12的Fe2+摄取系统(Feo)在小鼠肠道定殖中的作用。结果显示,Fe2+离子摄取受损的突变体在定殖能力方面也存在缺陷。产肠螯合素和不产肠螯合素的大肠杆菌feo突变体均无法在小鼠肠道定殖。这些结果表明,Fe(II)是肠道中生长的大肠杆菌铁的必需来源。

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