Roles of iron acquisition systems in virulence of extraintestinal pathogenic Escherichia coli: salmochelin and aerobactin contribute more to virulence than heme in a chicken infection model.
Roles of iron acquisition systems in virulence of extraintestinal pathogenic Escherichia coli: salmochelin and aerobactin contribute more to virulence than heme in a chicken infection model.
复制标题
铁获取系统在肠外致病性大肠杆菌毒力中的作用：在鸡感染模型中，沙莫螯合素和需氧菌素比血红素对毒力的贡献更大
DOI：
10.1186/1471-2180-12-143
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发表时间：
2012-07-20
期刊：
影响因子：
4.2
通讯作者：
Liu X
中科院分区：
文献类型：
--
作者：
Gao Q;Wang X;Xu H;Xu Y;Ling J;Zhang D;Gao S;Liu X
禽致病性大肠埃希菌(APEC)和尿路致病性大肠杆菌(UPEC)是肠外致病性大肠杆菌(ExPEC)的两个主要亚群。这两种类型都有多种铁获取系统，包括血红素和铁载体。尽管参与APEC或UPEC发病的铁转运系统已经在相应的动物模型中被单独记录，但这些系统在APEC和UPEC同时感染过程中的作用还没有得到很好的描述。构建了影响APEC E058和UPEC U17细胞铁摄取的等位基因突变株，并在鸡攻击模型中进行了比较。结果Salmochelin缺陷突变株E058ΔIrod和U17ΔIrod的致病性显著低于野生型菌株。Aerobactin缺陷突变体E058ΔiucD和U17ΔiucD在几个内脏器官的定植减少，而血红素缺陷突变体E058ΔChut和U17ΔChut在内脏的定植程度与其野生型菌株相同。E058和U17中的三个突变体ΔChutΔIrodΔiucD的致病力均低于单个突变体。用野生型毒株攻击的雏鸟内脏器官的组织病理学损伤比用ΔiROD、ΔiucD或三重突变体攻击的雏鸟严重。相反，接种ΔChut突变体的鸡与接种野生型菌株的鸡的皮损相似。但突变体和野生型菌株在抗血清能力、HD-11的细胞侵袭和细胞内存活以及在富铁和限铁介质中的生长等方面没有显著差异。Salmochelin和Aerobactin系统似乎在APEC和UPEC的毒力中都很重要，而Salmochelin对毒力的贡献更大。在这个模型中，由周质中的Chut结合的血红素似乎是多余的，这表明其他周质结合蛋白可能与观察到的血红素吸收突变体的无表型有关。在其他表型性状上，突变体与其野生型亲本之间没有差异，这表明其他毒力机制补偿了突变的影响。
BackgroundAvian pathogenic Escherichia coli (APEC) and uropathogenic E. coli (UPEC) are the two main subsets of extraintestinal pathogenic E. coli (ExPEC). Both types have multiple iron acquisition systems, including heme and siderophores. Although iron transport systems involved in the pathogenesis of APEC or UPEC have been documented individually in corresponding animal models, the contribution of these systems during simultaneous APEC and UPEC infection is not well described. To determine the contribution of each individual iron acquisition system to the virulence of APEC and UPEC, isogenic mutants affecting iron uptake in APEC E058 and UPEC U17 were constructed and compared in a chicken challenge model.ResultsSalmochelin-defective mutants E058ΔiroD and U17ΔiroD showed significantly decreased pathogenicity compared to the wild-type strains. Aerobactin defective mutants E058ΔiucD and U17ΔiucD demonstrated reduced colonization in several internal organs, whereas the heme defective mutants E058ΔchuT and U17ΔchuT colonized internal organs to the same extent as their wild-type strains. The triple mutant ΔchuTΔiroDΔiucD in both E058 and U17 showed decreased pathogenicity compared to each of the single mutants. The histopathological lesions in visceral organs of birds challenged with the wild-type strains were more severe than those from birds challenged with ΔiroD, ΔiucD or the triple mutants. Conversely, chickens inoculated with the ΔchuT mutants had lesions comparable to those in chickens inoculated with the wild-type strains. However, no significant differences were observed between the mutants and the wild-type strains in resistance to serum, cellular invasion and intracellular survival in HD-11, and growth in iron-rich or iron-restricted medium.ConclusionsResults indicated that APEC and UPEC utilize similar iron acquisition mechanisms in chickens. Both salmochelin and aerobactin systems appeared to be important in APEC and UPEC virulence, while salmochelin contributed more to the virulence. Heme bounded by ChuT in the periplasm appeared to be redundant in this model, indicating that other periplasmic binding proteins likely contributed to the observed no phenotype for the heme uptake mutant. No differences were observed between the mutants and their wild-type parents in other phenotypic traits, suggesting that other virulence mechanisms compensate for the effect of the mutations.