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Bacterial lactoferrin receptors

A B Schryvers1, R Bonnah, R H Yu

  • 1Department of Microbiology and Infectious Diseases, University of Calgary, Alberta, Canada.

Advances in Experimental Medicine and Biology
|October 22, 1998
PubMed
Summary
This summary is machine-generated.

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Lactoferrin binding proteins LbpA and FbpA are essential for bacterial iron acquisition. LbpB is not essential, while CopB is crucial for iron uptake from both lactoferrin and transferrin.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Iron Metabolism

Background:

  • Lactoferrin's antimicrobial function relies on iron sequestration.
  • Neisseriaceae bacteria possess surface receptors to acquire iron from lactoferrin.
  • Previous studies identified LbpA (100 kDa) and LbpB (84 kDa) as lactoferrin binding proteins.

Purpose of the Study:

  • To elucidate the roles of lactoferrin receptor proteins (LbpA, LbpB, CopB, FbpA) in bacterial iron acquisition.
  • To confirm the identities of lactoferrin binding proteins in Neisseriaceae.
  • To evaluate potential vaccine candidates among these receptors.

Main Methods:

  • Affinity isolation using immobilized lactoferrin.
  • Construction and analysis of isogenic mutants for lbpA, lbpB, CopB, and FbpA genes.

Related Experiment Videos

  • Growth studies to assess iron acquisition from lactoferrin.

    • Main Results:

    • LbpA and FbpA were essential for iron acquisition from lactoferrin.
    • LbpB was not essential, similar to bacterial transferrin receptors.
    • CopB-deficient mutants showed impaired iron acquisition from both transferrin and lactoferrin.
    • Convalescent antisera showed preferential reactivity with LbpB.

    Conclusions:

    • LbpA and FbpA are critical for lactoferrin iron uptake.
    • CopB plays a central role in iron acquisition from both transferrin and lactoferrin.
    • LbpB's non-essential role suggests alternative iron acquisition mechanisms.
    • LbpB is a potential vaccine antigen due to its surface accessibility and preferential antibody reactivity.