Acute iron overload in mice: pathogenesis of Salmonella typhimurium infection

Sawatzki, G.; Hoffmann, F.; Kubanek, B

doi:10.1128/iai.39.2.659-665.1983

Cited by 24 publications

(7 citation statements)

References 26 publications

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“…Studies have shown that iron availability is an important determinant of virulence. Mice with systemic iron deficiency are more resistant to infection (Puschmann and Ganzoni, 1977), whereas acute iron overload in mouse tissues results in enhanced bacterial outgrowth (Sawatzki et al, 1983). Nramp1+ mice are more resistant to infection than Nramp1− organisms (Vidal et al, 1995a,b).…”

Section: Iron Withholding and Acquisition In Host-pathogen Interactionsmentioning

confidence: 99%

The ins and outs of bacterial iron metabolism

Frawley

Fang

2014

Molecular Microbiology

155

106

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Summary Iron is a critical nutrient for the growth and survival of most bacterial species. Accordingly, much attention has been paid to the mechanisms by which host organisms sequester iron from invading bacteria and how bacteria acquire iron from their environment. However, under oxidative stress conditions such as those encountered within phagocytic cells during the host immune response, iron is released from proteins and can act as a catalyst for Fenton chemistry to produce cytotoxic reactive oxygen species. The transitory efflux of free intracellular iron may be beneficial to bacteria under such conditions. The recent discovery of putative iron efflux transporters in Salmonella enterica serovar Typhimurium is discussed in the context of cellular iron homeostasis.

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Section: Iron Withholding and Acquisition In Host-pathogen Interactionsmentioning

confidence: 99%

The ins and outs of bacterial iron metabolism

Frawley

Fang

2014

Molecular Microbiology

155

106

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“…Many of the genes required for Salmonella pathogenesis encode proteins involved in normal housekeeping functions of the cell. These include genes involved in DNA metabolism and amino acid biosynthesis, as well as genes involved in iron regulation (10,25) and stationary-phase growth (8,20). Mutations in these housekeeping genes can attenuate the virulence of Salmonella and allow the immune system to rapidly clear the infecting organisms.…”

Section: Fig 2 Survival Of S Typhimurium Derivatives In Murine Permentioning

confidence: 99%

Effect of mutS and recD Mutations on Salmonella Virulence

1999

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Hybrid derivatives of closely related bacteria may be used to dissect strain-specific functions that contribute to virulence within a host. However, mismatches between DNA sequences are a potent barrier to recombination. Recipients with mutS and recDmutations overcome this barrier, allowing construction of genetic hybrids. To determine whether Salmonella hybrids constructed in a mutS recD host can be used to study virulence, we assayed the effect of mutS andrecD mutations on the virulence of Salmonella typhimurium 14028s in mice. Mutants defective in eithermutS or recD do not affect the time course or the 50% lethal dose (LD50) of the infection. In contrast, the inactivation of both mutS and recD results in a synthetic phenotype which substantially increases the time required to cause a lethal infection without changing the LD50. This phenotype results from an inability ofmutS recD double mutants to rapidly adapt to purine-limiting conditions present within macrophages. Although the disease progression is slower, S. typhimurium mutS recDmutants retain the ability to cause lethal infections, and, thus, hybrids constructed in mutS recD hosts may permit the analysis of virulence factors in a surrogate animal model.

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“…A similar mechanism may act in mice homozygous for 13thalassemia. It is also possible that the excess tissue iron acts as a virulence factor for L. monocytogenes and S. typhimurium, both of which display increased growth under conditions of excess iron (5, 23,25,28). Excess tissue iron stores have been shown to enhance the pathogenicity of other intracellular pathogens (13,14).…”

Section: Discussionmentioning

confidence: 99%

Resistance to infection in murine beta-thalassemia

et al. 1989

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Clinical evidence suggests that individuals with chronic iron overload may be at increased risk of bacterial infection. We studied this question by using a unique model in which mice homozygous for a deletion in the gene encoding for the a-major globin develop moderate anemia, splenomegaly, and tissue iron overload, a syndrome similar to 0-thalassemia in humans. Mice heterozygous for the gene deletion were phenotypically normal. Homozygous mice were significantly more susceptible to infection with Listeria monocytogenes than were heterozygous mice (P < 0.01). This increased susceptibility was associated with a greater number of organisms in the liver and spleen than was found in heterozygous mice (P < 0.05). However, histologic studies demonstrated similar inflammatory responses within these organs in homozygous and heterozygous mice. The increased susceptibility of homozygous mice to infection with L. monocytogenes was not seen when homozygotes were immunized with a low dose of L. monocytogenes. Although the results were not as striking as with L. monocytogenes, homozygous mice were also found to be more susceptible to infection with Salmonella

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Acute iron overload in mice: pathogenesis of Salmonella typhimurium infection

Cited by 24 publications

References 26 publications

The ins and outs of bacterial iron metabolism

The ins and outs of bacterial iron metabolism

Effect of mutS and recD Mutations on Salmonella Virulence

Resistance to infection in murine beta-thalassemia

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