Knocking on the right door and making a comfortable home: Histoplasma capsulatum intracellular pathogenesis.
Histoplasma capsulatum is a successful intracellular pathogen of mammalian macrophages. As such, this fungus must survive and/or subvert hostile environmental onslaughts in a professionally antimicrobial host cell. H. capsulatum uses different host receptors for binding to macrophages (beta 2 integrins) than it uses for binding to dendritic cells (the fibronectin receptor); the fungus experiences different degrees of success in survival in these two cells. Surface expression of HSP60 as the specific adhesin for macrophage beta 2 integrins represents a novel mechanism for binding. Long considered a resident of the phagolysosome, H. capsulatum may also reside in a modified phagosome without experiencing phagolysosomal fusion. H. capsulatum must compete with the host to acquire the essential nutrient iron, and has several potential mechanisms for accomplishing this necessary feat. Finally, H. capsulatum displays morphotype-specific expression of several genes, and a calcium-binding protein expressed only by the pathogenic yeast phase has been demonstrated as essential for full virulence. An organism's environment is of great importance to its success or failure, and H. capsulatum is good at finding or making the right environment in the host.
Woods
Jon P
JP
Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, 1300 University Avenue, 420 SMI, Madison, WI 53706-1532, USA. jpwoods@wisc.edu
D000818:Animals; D006658:Histoplasma / Q000254:growth & development / Q000378:metabolism* / Q000472:pathogenicity*; D006660:Histoplasmosis / Q000382:microbiology*; D006801:Humans; D007501:Iron / Q000378:metabolism; D014774:Virulence
D007501:Iron