Iron uptake mechanisms of pathogenic bacteria

Authors

  • Karl G. Wooldridge,

    1. Department of Genetics, University of Leicester, Leicester, UK
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    • *

      We are grateful to Elwyn Griffiths, Paul Williams, Jorge Crosa, Colin Ratledge, Pete Borriello and Rolf Reissbrodt for providing manuscripts prior to publication. We also thank Julian Ketley for helpful comments and discussions.

  • Peter H. Williams

    Corresponding author
    1. Department of Genetics, University of Leicester, Leicester, UK
      *Correspondence to: P.H. Williams, Department of Genetics, University of Leicester, Leicester LEl 7RH, UK.
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    • *

      We are grateful to Elwyn Griffiths, Paul Williams, Jorge Crosa, Colin Ratledge, Pete Borriello and Rolf Reissbrodt for providing manuscripts prior to publication. We also thank Julian Ketley for helpful comments and discussions.


*Correspondence to: P.H. Williams, Department of Genetics, University of Leicester, Leicester LEl 7RH, UK.

Abstract

Abstract: Most of the iron in a mammalian body is complexed with various proteins. Moreover, in response to infection, iron availability is reduced in both extracellular and intracellular compartments. Bacteria need iron for growth and successful bacterial pathogens have therefore evolved to compete successfully for iron in the highly iron-stressed environment of the host's tissues and body fluids. Several strategies have been identified among pathogenic bacteria, including reduction of ferric to ferrous iron, occupation of intracellular niches, utilisation of host iron compounds, and production of siderophores. While direct evidence that high affinity mechanisms for iron acquisition function as bacterial virulence determinants has been provided in only a small number of cases, it is likely that many if not all such systems play a central role in the pathogenesis of infection.

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