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

Stojiljkovic, I

doi:10.1016/0378-1097(93)90496-o

Cited by 19 publications

(23 citation statements)

References 9 publications

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“…This stagnation in competition could encourage extended plasmid persistence and might be explained by changes in the growth rate of gut inhabiting strains over time; indicating a non-constant selection pattern (Rang et al, 1999). Such selection patterns are known to occur in mixed bacterial populations encompassing social iron acquisition phenotypes and similar dynamics could take place in the competition between pNK29-2 carrying and plasmid-free strains in the gut (Stojiljkovic et al, 1993; Ross-gillespie et al, 2007). However, this does not seem to be the case from our growth rate measurements in iron-limiting conditions, were the plasmid carrying strain did not have an advantage on its own (Figure S3).…”

Section: Discussionmentioning

confidence: 94%

Genome Dynamics of Escherichia coli during Antibiotic Treatment: Transfer, Loss, and Persistence of Genetic Elements In situ of the Infant Gut

Porse

Gumpert

Kubicek-Sutherland

et al. 2017

Front. Cell. Infect. Microbiol.

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Elucidating the adaptive strategies and plasticity of bacterial genomes in situ is crucial for understanding the epidemiology and evolution of pathogens threatening human health. While much is known about the evolution of Escherichia coli in controlled laboratory environments, less effort has been made to elucidate the genome dynamics of E. coli in its native settings. Here, we follow the genome dynamics of co-existing E. coli lineages in situ of the infant gut during the first year of life. One E. coli lineage causes a urinary tract infection (UTI) and experiences several alterations of its genomic content during subsequent antibiotic treatment. Interestingly, all isolates of this uropathogenic E. coli strain carried a highly stable plasmid implicated in virulence of diverse pathogenic strains from all over the world. While virulence elements are certainly beneficial during infection scenarios, their role in gut colonization and pathogen persistence is poorly understood. We performed in vivo competitive fitness experiments to assess the role of this highly disseminated virulence plasmid in gut colonization, but found no evidence for a direct benefit of plasmid carriage. Through plasmid stability assays, we demonstrate that this plasmid is maintained in a parasitic manner, by strong first-line inheritance mechanisms, acting on the single-cell level, rather than providing a direct survival advantage in the gut. Investigating the ecology of endemic accessory genetic elements, in their pathogenic hosts and native environment, is of vital importance if we want to understand the evolution and persistence of highly virulent and drug resistant bacterial isolates.

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Section: Discussionmentioning

confidence: 94%

Genome Dynamics of Escherichia coli during Antibiotic Treatment: Transfer, Loss, and Persistence of Genetic Elements In situ of the Infant Gut

Porse

Gumpert

Kubicek-Sutherland

et al. 2017

Front. Cell. Infect. Microbiol.

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“…The Feo transport system is found in most bacteria, and in the Enterobacteriaceae it is encoded by the feoABC operon [62–64]. FeoB is a cytoplasmic membrane protein with multiple membrane-spanning regions predicted to form the channel for iron transport.…”

Section: Ferrous Iron Transportmentioning

confidence: 99%

Regulation of iron transport systems in Enterobacteriaceae in response to oxygen and iron availability

Carpenter

Payne

2014

Journal of Inorganic Biochemistry

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Iron is an essential nutrient for most bacteria. Depending on the oxygen available in the surrounding environment, iron is found in two distinct forms: ferrous (FeII) or ferric (FeIII). Bacteria utilize different transport systems for the uptake of the two different forms of iron. In oxic growth conditions, iron is found in its insoluble, ferric form, and in anoxic growth conditions iron is found in its soluble, ferrous form. Enterobacteriacea, have adapted to transporting the two forms of iron by utilizing the global, oxygen-sensing regulators, ArcA and Fnr to regulate iron transport genes in response to oxygen.

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“…24 In many bacterial species, the Feo system ( feoABC ) mediates Fe(II) uptake. 25,26 Extracellular Fe(II) can be abundant under oxygen-limiting conditions, 27 and the Feo system has been implicated in the survival and virulence of bacterial pathogens that can inhabit low-oxygen microenvironments in the host, including Pseudomonas aerugionsa , 28,29 Helicobacter pylori , 30 Campylobacter jejuni , 31 Streptococcus suis, 32 and the obligate anaerobe Clostridium perfringens . 33 In addition to using the Fe(II) permease FeoB for Fe acquisition, the opportunistic human pathogen Pseudomonas aeruginosa produces and releases redox-cycling secondary metabolites named phenazines that reduce Fe(III) to Fe(II) in the extracellular environment and therefore proposed to facilitate Fe uptake via FeoB.…”

Section: Introductionmentioning

confidence: 99%

Human calprotectin affects the redox speciation of iron

Nakashige

Nolan

2017

Metallomics

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We report that the metal-sequestering human host-defense protein calprotectin (CP, S100A8/S100A9 oligomer) affects the redox speciation of iron (Fe) in bacterial growth media and buffered aqueous solution. Under aerobic conditions and in the absence of an exogenous reducing agent, CP-Ser (S100A8(C42S)/S100A9(C3S) oligomer) depletes Fe from three different bacterial growth media preparations over a 48-h timeframe (T = 30 °C). The presence of the reducing agent β-mercaptoethanol accelerates this process and allows CP-Ser to deplete Fe over a ≈1-h timeframe. Fe-depletion assays performed with metal-binding-site variants of CP-Ser show that the hexahistidine (His6) site, which coordinates Fe(II) with high affinity, is required for Fe depletion. An analysis of Fe redox speciation in buffer containing Fe(III) citrate performed under aerobic conditions demonstrates that CP-Ser causes a time-dependent increase in the [Fe(II)]/[Fe(III)] ratio. Taken together, these results indicate that the hexahistidine site of CP stabilizes Fe(II) and thereby shifts the redox equilibrium of Fe to the reduced ferrous state under aerobic conditions. We also report that the presence of bacterial metabolites affects the Fe-depleting activity of CP-Ser. Supplementation of bacterial growth media with an Fe(III)-scavenging siderophore (enterobactin, staphyloferrin B, or desferrioxamine B) attenuates the Fe-depleting activity of CP-Ser. This result indicates that formation of Fe(III)-siderophore complexes blocks CP-mediated reduction of Fe(III) and hence the ability of CP to coordinate Fe(II). In contrast, the presence of pyocyanin (PYO), a redox-cycling phenazine produced by Pseudomonas aeruginosa that reduces Fe(III) to Fe(II), accelerates Fe depletion by CP-Ser under aerobic conditions. These findings indicate that the presence of microbial metabolites that contribute to metal homeostasis at the host/pathogen interface can affect the metal-sequestering function of CP.

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

Cited by 19 publications

References 9 publications

Genome Dynamics of Escherichia coli during Antibiotic Treatment: Transfer, Loss, and Persistence of Genetic Elements In situ of the Infant Gut

Genome Dynamics of Escherichia coli during Antibiotic Treatment: Transfer, Loss, and Persistence of Genetic Elements In situ of the Infant Gut

Regulation of iron transport systems in Enterobacteriaceae in response to oxygen and iron availability

Human calprotectin affects the redox speciation of iron

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