Sigel S P, Stoebner J A, Payne S M
Infect Immun. 1985 Feb;47(2):360-2. doi: 10.1128/iai.47.2.360-362.1985.
The possible requirement of a functional siderophore (vibriobactin)-mediated iron transport system in the pathogenicity of Vibrio cholerae was determined. Two mutants of V. cholerae defective in the iron-vibriobactin transport system were examined for their ability to multiply and elicit diarrhea in infant mice. One mutant, 40130, was unable to synthesize vibriobactin. The second mutant, 1510, was able to synthesize, but not transport, the siderophore. Both mutants retained the ability to multiply and produce disease in the infant mouse, and virulence was indistinguishable from the parent strains. This indicates that a functional iron-vibriobactin transport system is not essential for cholera pathogenesis. These mutants, like the wild-type strains, were found to have a ferric citrate iron uptake system and could utilize citrate or asparagine for growth in low-iron medium. Compounds of this type may increase the availability of iron to V. cholerae in the host.
确定了功能性铁载体(弧菌素)介导的铁转运系统在霍乱弧菌致病性中可能的需求。检测了两株铁-弧菌素转运系统有缺陷的霍乱弧菌突变体在幼鼠体内繁殖和引发腹泻的能力。一个突变体40130无法合成弧菌素。第二个突变体1510能够合成但不能转运铁载体。这两个突变体在幼鼠体内均保留了繁殖和致病的能力,其毒力与亲本菌株无差异。这表明功能性铁-弧菌素转运系统对霍乱发病机制并非必不可少。这些突变体与野生型菌株一样,具有柠檬酸铁摄取系统,并且可以利用柠檬酸盐或天冬酰胺在低铁培养基中生长。这类化合物可能会增加霍乱弧菌在宿主体内获取铁的能力。