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Endogenous hepcidin and its agonist mediate resistance to selected infections by clearing non-transferrin-bound iron

Deborah Stefanova1, Antoan Raychev2, Joao Arezes3

  • 1Molecular, Cellular, and Integrative Physiology Graduate Program and.

Blood
|May 4, 2017
PubMed

Insights

The hormone hepcidin protects against siderophilic bacteria by controlling non-transferrin-bound iron (NTBI). This finding suggests hepcidin analogs could treat specific bacterial infections.

Area of Science:

  • Immunology
  • Microbiology
  • Hematology

Background:

  • The iron-regulatory hormone hepcidin influences host defense during infection by sequestering iron.
  • The precise mechanisms and microbial targets of hepcidin-mediated immunity remain unclear.
  • Hepcidin's role in modulating iron availability for microbial pathogens requires further investigation.

Purpose of the Study:

  • To elucidate the mechanisms by which hepcidin and hypoferremia impact host defense against diverse microbial pathogens.
  • To determine the specific role of non-transferrin-bound iron (NTBI) in bacterial growth during infection.
  • To assess the potential therapeutic applications of hepcidin modulation for infectious diseases.

Main Methods:

  • Utilized mouse models of infection to study hepcidin's effects on host defense.
  • Investigated the impact of hepcidin and iron overload on the growth of various bacterial species, including siderophilic and nonsiderophilic pathogens.
  • Analyzed the role of non-transferrin-bound iron (NTBI) versus transferrin-bound iron in supporting bacterial replication.

Main Results:

  • Hepcidin conferred selective protection against siderophilic extracellular bacteria (Yersinia enterocolitica O9) by regulating NTBI levels.
  • Non-transferrin-bound iron significantly promoted the rapid growth of siderophilic bacteria in iron-overloaded conditions and human plasma.
  • Hepcidin modulation and iron loading did not broadly enhance intracellular infections (Mycobacterium tuberculosis) or affect nonsiderophilic extracellular bacteria (Y. enterocolitica O8, Staphylococcus aureus).

Conclusions:

  • Hepcidin's protective effect against certain bacterial infections is mediated through the control of non-transferrin-bound iron.
  • Non-transferrin-bound iron is a critical factor supporting the proliferation of siderophilic pathogens.
  • Hepcidin analogs represent a potential therapeutic strategy for treating infections caused by siderophilic bacteria.

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