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Knocking on the right door and making a comfortable home: Histoplasma capsulatum intracellular pathogenesis

Jon P Woods1

  • 1Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, 1300 University Avenue, 420 SMI, Madison, WI 53706-1532, USA. jpwoods@wisc.edu

Current Opinion in Microbiology
|August 28, 2003
PubMed

Insights

Histoplasma capsulatum invades macrophages by binding to specific receptors like beta 2 integrins. This fungus employs various strategies to survive within host cells, including iron acquisition and morphotype-specific gene expression for virulence.

Area of Science:

  • Mycology
  • Infectious Diseases
  • Cell Biology

Background:

  • Histoplasma capsulatum is an intracellular pathogen that infects mammalian macrophages.
  • Fungal survival within host cells requires subverting antimicrobial defenses.

Purpose of the Study:

  • To investigate the mechanisms of Histoplasma capsulatum interaction with host cells.
  • To identify fungal adhesins and survival strategies within macrophages and dendritic cells.

Main Methods:

  • Analysis of host receptor usage for fungal binding to macrophages and dendritic cells.
  • Investigation of intracellular lifestyle and iron acquisition mechanisms.
  • Examination of morphotype-specific gene expression and virulence factors.

Main Results:

  • H. capsulatum utilizes distinct receptors (beta 2 integrins for macrophages, fibronectin receptor for dendritic cells) for cell binding.
  • Surface-expressed HSP60 acts as a novel adhesin for macrophage beta 2 integrins.
  • The fungus may reside in modified phagosomes, avoiding phagolysosomal fusion.
  • Mechanisms for iron acquisition and the role of a yeast-phase specific calcium-binding protein in virulence were explored.

Conclusions:

  • H. capsulatum employs specific adhesion mechanisms and intracellular survival strategies to establish infection.
  • Differential host cell interactions and environmental adaptation are key to fungal pathogenesis.

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