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Published on: February 7, 2013

Histoplasma requires SID1, a member of an iron-regulated siderophore gene cluster, for host colonization

Lena H Hwang1, Jacob A Mayfield, Jasper Rine

  • 1Department of Microbiology and Immunology, University of California, San Francisco, California, United States of America.

Plos Pathogens
|April 12, 2008
PubMed

Insights

Histoplasma capsulatum uses siderophores for iron acquisition during infection. Disrupting the SID1 gene impaired fungal growth in macrophages and reduced virulence in a mouse model.

Area of Science:

  • Medical Mycology
  • Molecular Pathogenesis
  • Fungal Genetics

Background:

  • Macrophages are primary hosts for Histoplasma capsulatum during infection.
  • Iron acquisition is crucial for pathogen virulence, yet its role in H. capsulatum remains unclear.
  • Key genes for iron acquisition and their contribution to virulence are largely unknown.

Purpose of the Study:

  • Investigate the role of iron acquisition in Histoplasma capsulatum pathogenesis.
  • Identify and characterize genes involved in iron acquisition, particularly siderophore synthesis and utilization.
  • Determine the contribution of these genes to fungal growth and virulence within the host.

Main Methods:

  • Transcriptional analysis of H. capsulatum under low-iron conditions.
  • Genomic analysis to identify co-regulated iron acquisition genes and promoter sequences.
  • Gene disruption via allelic replacement to study the function of SID1.
  • In vitro growth assays in murine bone-marrow-derived macrophages.
  • In vivo virulence assessment using a mouse model of infection.

Main Results:

  • Identified a cluster of co-regulated genes involved in siderophore synthesis, secretion, and utilization, induced under low iron.
  • Discovered a consensus promoter sequence potentially regulating iron-dependent gene expression.
  • Disruption of L-ornithine monooxygenase (SID1) abolished siderophore production and impaired growth in low iron.
  • SID1-deficient strains exhibited significant growth defects in macrophages and reduced virulence in mice.

Conclusions:

  • Histoplasma capsulatum employs siderophores as a critical mechanism for iron acquisition during mammalian infection.
  • The SID1 gene is essential for siderophore production and contributes to H. capsulatum's virulence.
  • Coordinate regulation of siderophore-related genes, possibly via genomic proximity and promoter elements, facilitates iron acquisition.

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