Freestone Primrose P E, Haigh Richard D, Williams Peter H, Lyte Mark
Department of Microbiology and Immunology, University of Leicester, Leicester, UK.
FEMS Microbiol Lett. 2003 May 16;222(1):39-43. doi: 10.1016/S0378-1097(03)00243-X.
Exposure of bacteria to members of the stress-associated family of catecholamine hormones, principally norepinephrine, has been demonstrated to increase both growth and production of virulence-related factors. Mutation of genes for enterobactin synthesis and uptake revealed an absolute requirement for enterobactin in norepinephrine-stimulated growth of Escherichia coli O157:H7. The autoinducer produced by norepinephrine-stimulated E. coli could not substitute for enterobactin. We also demonstrate that norepinephrine promotes iron shuttling between transferrin molecules, thereby enabling the bacterial siderophore enterobactin to more readily acquire iron for growth. These results suggest one of the possible mechanisms by which the hormonal output of stress may affect enterohaemorrhagic E. coli pathogenicity.
已证明,细菌暴露于与应激相关的儿茶酚胺激素家族成员(主要是去甲肾上腺素)中,会增加其生长以及与毒力相关因子的产生。肠杆菌素合成和摄取基因的突变表明,在去甲肾上腺素刺激的大肠杆菌O157:H7生长过程中,对肠杆菌素存在绝对需求。去甲肾上腺素刺激的大肠杆菌产生的自诱导物无法替代肠杆菌素。我们还证明,去甲肾上腺素可促进转铁蛋白分子之间的铁穿梭,从而使细菌铁载体肠杆菌素更易于获取铁以供生长。这些结果提示了应激激素输出可能影响肠出血性大肠杆菌致病性的一种可能机制。