Iron metabolism: microbes, mouse, and man

Latunde-Dada, Gladys O.

doi:10.1002/bies.200900101

Cited by 25 publications

(29 citation statements)

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“…The correlation between iron acquisition and bacterial virulence has been well documented [3], [4], [5] and the absolute requirement for this metal for both host metabolism and bacterial growth results in significant competition for iron in the host [6]. Following bacterial infection host responses are evoked which sequester iron, making it relatively unavailable for bacterial metabolism [7].…”

Section: Introductionmentioning

confidence: 99%

A Putative P-Type ATPase Required for Virulence and Resistance to Haem Toxicity in Listeria monocytogenes

et al. 2012

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Regulation of iron homeostasis in many pathogens is principally mediated by the ferric uptake regulator, Fur. Since acquisition of iron from the host is essential for the intracellular pathogen Listeria monocytogenes, we predicted the existence of Fur-regulated systems that support infection. We examined the contribution of nine Fur-regulated loci to the pathogenicity of L. monocytogenes in a murine model of infection. While mutating the majority of the genes failed to affect virulence, three mutants exhibited a significantly compromised virulence potential. Most striking was the role of the membrane protein we designate FrvA (Fur regulated virulence factor A; encoded by frvA [lmo0641]), which is absolutely required for the systemic phase of infection in mice and also for virulence in an alternative infection model, the Wax Moth Galleria mellonella. Further analysis of the ΔfrvA mutant revealed poor growth in iron deficient media and inhibition of growth by micromolar concentrations of haem or haemoglobin, a phenotype which may contribute to the attenuated growth of this mutant during infection. Uptake studies indicated that the ΔfrvA mutant is unaffected in the uptake of ferric citrate but demonstrates a significant increase in uptake of haem and haemin. The data suggest a potential role for FrvA as a haem exporter that functions, at least in part, to protect the cell against the potential toxicity of free haem.

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Section: Introductionmentioning

confidence: 99%

A Putative P-Type ATPase Required for Virulence and Resistance to Haem Toxicity in Listeria monocytogenes

et al. 2012

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“…It then acts as pivotal iron regulatory hormone and a pleiotropic sensor of divalent metals that shifts the iron from circulation into cellular stores in hepatocytes and macrophages, attenuating intestinal iron absorption and a macrophage iron release [47,48]. This might be favorable in inflammation and in cancer, since this makes iron less available for invading microorganisms and growth of tumor cells [38] but is also harmful, owing to the resultant hypoferremia which concomitantly might damage several functions in the host [49].…”

Section: Discussionmentioning

confidence: 98%

Kinetics of Tissue Iron in Experimental Autoimmune Encephalomyelitis in Rats

Tota

Jakovac

Grebić

et al. 2010

Biol Trace Elem Res

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To elucidate the role of iron in the pathomechanisms of autoimmune CNS disorders, we estimated the tissue concentrations of Fe(2+) in the brain, spinal cord, and liver in the chronic relapsing form of experimental autoimmune encephalomyelitis (EAE). The disease was induced in Dark Agouti (DA) strain of rats, by subcutaneous injection of bovine brain homogenate in complete Freund's adjuvant (CFA). Control rats consisted of unsensitized rats and of rats treated with CFA or saline. The data obtained by clinical assessment and by inductively coupled plasma spectrometry have shown that the attacks of disease (on the 12th and 22nd post-immunization day) were followed by high accumulation of iron in the liver. Additionally, during the second attack of disease, the decreased concentration of Fe(2+) was found in cervical spinal cord. The data point to regulatory effects of iron and hepatic trace elements regulating mechanisms in the pathogenesis of EAE.

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“…Since those special environments enriched in trace elements are also often colonized with bacterial pathogens, it is of prime importance to understand whether such trace metal levels affect the metabolism and virulence factors expression of bacterial pathogens. A link between iron availability in the host and bacterial virulence has long been established (for reviews [7,8]). There is an increasing body of evidence, however, that several other metals such as Zn, Cu or Ni might also play a role in bacterial virulence [9e12], and might function as a selective pressure for antibiotic resistance, affecting the treatment of infectious diseases [13].…”

Section: Introductionmentioning

confidence: 99%