How pathogenic bacteria evade mammalian sabotage in the battle for iron

被引:242
作者
Fischbach, MA
Lin, HN
Liu, DR
Walsh, CT
机构
[1] Harvard Univ, Sch Med, Dept Biol Chem & Mol Pharmacol, Boston, MA 02115 USA
[2] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA
[3] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA
[4] Harvard Univ, Sch Med, Dept Biol Chem, Boston, MA 02115 USA
[5] Harvard Univ, Sch Med, Dept Mol Pharmacol, Boston, MA 02115 USA
[6] Harvard Univ, Howard Hughes Med Inst, Cambridge, MA 02138 USA
[7] Harvard Univ, Dept Chem & Chem Biol, Cambridge, MA 02138 USA
关键词
D O I
10.1038/nchembio771
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
Many bacteria, including numerous human pathogens, synthesize small molecules known as siderophores to scavenge iron. Enterobactin, a siderophore produced by enteric bacteria, is surprisingly ineffective as an iron-scavenging agent for bacteria growing in animals because of its hydrophobicity and its sequestration by the mammalian protein siderocalin, a component of the innate immune system. However, pathogenic strains of Escherichia coli and Salmonella use enzymes encoded by the iroA gene cluster to tailor enterobactin by glycosylation and linearization. The resulting modified forms of enterobactin, known as salmochelins, can evade siderocalin and are less hydrophobic than enterobactin, restoring this siderophore's iron-scavenging ability in mammals.
引用
收藏
页码:132 / 138
页数:7
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