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PubMed1978

Uptake of metabolites by germinating blastospores of Histoplasma capsulatum.

The uptake of radioactive L-leucine, L-glutamic acid, and guanine was monitored during blastospore germination of Histoplasma capsulatum. Blastospores of H. capsulatum, grown in Salvin's medium at 37 degrees C for 48 h and shifted to 23 degrees C, germinated within 24 h. Metabolite uptake was faster in mycelial cells at 23 degrees C than it was in yeast cells at 37 degrees C. During the yeast to mold transition, the initial rate of uptake was first markedly depressed and then increased and achieved a level characteristic of the mycelial phase of growth. Estimates of macromolecular synthesis occurring during transitional morphological events might be influenced by these differences in the rate of uptake.

Culture Media↗
PubMed1978

Histoplasma capsulatum: chemical variability of the yeast cell wall.

Four strains of Histoplasma capsulatum were analyzed to observe any variations in their cell wall composition. Strain G-184B produced the same amount of sugars reported by Domer (2) although qualitative analyses agreed with Kanetsuna's report (4) as far as the presence of glucose, galactose, and mannose was concerned. Our results agree with previous reports in classifying H. capsulatum into chemotypes I and II, the latter having more alpha-glucan in its cell wall. A decrease in the amount of fraction 2 (alpha-glucan) of strain G-184B was observed when the strain was subcultured in vitro for many years, an effect similar to that reported for Paracoccidioides brasiliensis (12, 13).

Cell Wall↗
PubMed1979

Cysteine biosynthesis in a fungus, Histoplasma capsulatum.

We have analyzed a step in cysteine biosynthesis in several strains of the pathogenic dimorphic fungus, Histoplasma capsulatum. Mycelial cells of all strains tested are prototrophic. However, the yeast phase cells of most stains do not grow in the absence of -SH-containing compounds due to the apparent lack of an active form of sulfite reductase, a crucial enzyme in the cysteine biosynthetic pathway. In contrast, the yeast phase cells of one strain (Downs) have been found to have an active sulfite reductase and can grow in the absence of cysteine if serine is added. A different metabolic block must thus exist in this strain. Sulfite reductase in the yeast form of Downs strain is completely repressed by growth on cysteine while the mycelial form seems to be constitutive. The yeast and mycelial phase extracts were analyzed on polyacrylamide gels. A distinct protein band appeared in extracts prepared from the yeast cells incubated in minimal or serine-containing media, but not in extracts from mycelia or from cysteine-grown yeast cells.

Chloramphenicol↗
PubMed1981

Ultrastructural studies on the dimorphism of Paracoccidioides brasiliensis, Blastomyces dermatitidis and Histoplasma capsulatum.

Whole cells or cell walls of the yeastlike and mycelial forms of Paracoccidioides brasiliensis, Blastomyces dermatitidis and Histoplasma capsulatum were treated successively with sodium hydroxide, beta-1,3-glucanase and pronase. The microfibrils in the insoluble residues, probably composed of chitin, were examined in the electron microscope. In the yeastlike form, tightly interwoven, randomly oriented microfibrils were seen. On the other hand, in the mycelial form, a large portion of microfibrils tended to lie in a more or less longitudinal orientation. A role of chitin in the conversion from the yeastlike form to the mycelial form is discussed.

Blastomyces↗
PubMed1983

Study of equine histoplasmosis farciminosi and characterization of Histoplasma farciminosum.

A detailed clinical and mycological study of horse infections with Histoplasma farciminosum was conducted for the first time in the Middle East. The disease seems to prevail in endemic form in the region. In all of the cases studied the infection involved only the cutaneous lymphatics and skin tissue with extension to the regional draining lymph glands. The disease seems to impose serious economic impact in the infected areas. Full description and thorough characterization of both the mycelial form and the yeast phase of the causative fungus were made.

Animals↗
PubMed1994

Immunochemical studies of heat-shock protein 80 of Histoplasma capsulatum.

A monoclonal antibody (MAb) of the IgG1 subclass, with greater activity to the yeast than the mycelial phase of Histoplasma capsulatum was raised and was found to predominantly recognize a molecule of 80 kDa by immunoblot. Enzymatic deglycosylation and chemical degradation, followed by reaction with MAb 69F on Western blots showed the molecule to be O-glycosylated, and immunofluorescence studies showed it to be heat-inducible and its distribution to be cytoplasmic and possibly cell membraneous. There was no apparent staining of the cell wall. Culture filtrate was positive by ELISA and Western blot when reacted with MAb 69F. In addition, ELISA and Western blot demonstrated that a similar epitope was present in other fungal species. The glycoprotein had a pI of approximately 4.7. N-terminal amino acid sequencing revealed this molecule to be homologous to members of the heat-shock protein 70 family and to a recently described antigen from H. capsulatum.

Amino Acid Sequence↗
PubMed2004

Histoplasma capsulatum yeast cells attach and agglutinate human erythrocytes.

The ability of yeast cells of Histoplasma capsulatum to attach and agglutinate human erythrocytes has been described. This is the first report involving these yeasts in the hemagglutination phenomenon. Results revealed that the yeast cells were able to bind to erythrocytes irrespective of blood groups and to agglutinate them when a high density of yeast cells was used. Assays on the inhibition of yeast attachment to erythrocytes were also performed, using sugar-treated yeast cells. Results indicate that galactose (Gal), mainly the beta-anomer, specially inhibited yeast attachment. Disaccharides (Gal-derivatives) and glycosaminoglycans containing Gal residues, mainly chondroitin sulfate C, promote this type of inhibition. In addition, preliminary data of inhibition assays also involved a probable ionic strength driven mechanism mediated by sialic acid and heparan sulfate, suggesting that yeast binding to erythrocytes could be associated with negative charges of both molecules.

Blood Group Antigens↗
PubMed2005

Chrysosporium chiropterorum sp. nov., isolated in France, resembling Chrysosporium state of Ajellomyces capsulatus (Histoplasma capsulatum).

A fungus isolated in France from the fur of a bat, which produces characterized large tuberculate conidia (aleurioconidia) similar to those produced by the mycelial form of Histoplasma capsulatum (Ajellomyces capsulatus) is described. Colonies are white at first, but then become rosy buff from the centre outwards. Sectoring, resulting in the appearance of patches or areas of dark green mycelium, occurs spontaneously. Single-celled conidia are formed on undifferentiated hyphae, and may be sessile, or borne laterally on short stalks or producing in an intercalary position as it is the case in the genus Chrysosporium. This fungus is clearly distinguishable from any described species and is described as Chrysosporium chiropterorum sp. nov. C. chiropterorum, like H. capsulatum, produces gelatinase, and is non-keratinolytic but strongly ureolytic. Both species are associated with bat dwellings. C. chiropterorum differs from H. capsulatum by faster growth, pink or green colonies, and failure to produce microconidia as well as lack of conversion to a yeast phase in vitro at 37 degrees C.

Animals↗
PubMed2000

Monitoring internalization of Histoplasma capsulatum by mammalian cell lines using a fluorometric microplate assay.

We have developed a fluorometric microtiter plate assay to quantify the internalization of Histoplasma capsulatum yeasts by macrophages. The assay utilizes the fluorescent dye Calcofluor White to label the yeast cell wall and the vital dye trypan blue, which does not enter viable macrophages, to quench fluorescence of extracellular labeled yeasts. Murine RAW 264.7 cells showed more efficient internalization of strain G217B yeasts than human U937 cells. Both cell lines exhibited a dependence upon actin, and, to a lesser degree, microtubules, in G217B uptake.

Animals↗
PubMed2000

Host response and Histoplasma capsulatum/macrophage molecular interactions.

Histoplasma capsulatum is the etiological agent of histoplasmosis, a chronic respiratory infection that is generally asymptomatic in healthy individuals, but severe or fatal in patients who are immunosuppressed or otherwise debilitated. H. capsulatum is found as a mould in soil and becomes a pathogenic yeast in the mammalian host. The first line of defense that H. capsulatum faces during host invasion is the attack of polymorphonuclear neutrophils and resident macrophages. In animal models, once phagocytosed, H. capsulatum is not killed by fusion of the phago-lysosomes, instead it multiplies within non-activated macrophages and destroys them. Upon induction of cell-mediated immunity, cytokines activate macrophages and destroy the yeast cells. Some aspects of the fungus-macrophage interaction have been elucidated, and it is clear that some of the mechanisms by which H. capsulatum escapes the lethal effects of this very hostile environment, involve the regulation of specific genes. Recently, using the differential display reverse transcriptase polymerase chain reaction technique, a number of H. capsulatum genes that are induced after the yeasts are ingested by macrophages have been identified. However, the mechanisms that underlie the capacity of H. capsulatum to adapt to the new environmental conditions present in macrophages remain to be clarified.

Animals↗
PubMed2002

Functional properties of the T cell receptor repertoire in responding to the protective domain of heat-shock protein 60 from Histoplasma capsulatum.

Cells expressing the T cell receptor beta-chain variable region (Vbeta) 6 constitute the majority of T cells responding to the protective domain (F3) of heat-shock protein 60 from Histoplasma capsulatum. This subset of cells exhibits a T helper type 1 (Th1) profile and is pivotal in protection. In this study, additional F3-reactive T cell lines were generated, leading to the discovery of a Th2 line. Vbeta usage by clones was more diverse than has been previously recognized. Nearly all Th2 clones expressed Vbeta8.1/8.2, whereas Th1 clones expressed Vbeta11 or Vbeta6. In adoptive transfer studies, only the Vbeta6(+) Th1 clone prolonged survival; all Th2 clones accelerated mortality. The ameliorative effect of the Vbeta6(+) Th1 clone was abrogated by treatment with monoclonal antibody to interferon-gamma. Neutralization of interleukin-4 reversed the shortened survival of mice to which the Vbeta6(+) Th2 clone was administered. Thus, F3-mediated protection is confined to a defined Vbeta population, but exacerbation of disease is mediated by multiple Vbeta families.

Adoptive Transfer↗
PubMed2005

Modulation of infection with Histoplasma capsulatum by inhibition of tumor necrosis factor-alpha activity.

Tumor necrosis factor (TNF)-alpha is required for host defenses against a number of pathogenic microbes, including Histoplasma capsulatum. In mice, TNF-alpha is necessary for the generation of a protective immune response to both primary and secondary histoplasmosis. Recent reports indicate that, in humans, treatment with inhibitors of TNF-alpha is associated with disseminated histoplasmosis. Here, I review the mechanisms by which inhibition of TNF-alpha may exacerbate infection with H. capsulatum.

Animals↗
PubMed2005

T cells require tumor necrosis factor-alpha to provide protective immunity in mice infected with Histoplasma capsulatum.

We examined whether neutralization of tumor necrosis factor (TNF)-alpha after intranasal exposure of mice to Histoplasma capsulatum was necessary for control of primary or secondary infection. All mice given monoclonal antibody to TNF-alpha on the day of infection or on day 3 after infection died. When antibody was administered on day 5 after infection, 60% of mice with primary infection died, whereas none with secondary infection did. Antibody treatment on day 7 after infection produced a transiently higher fungal burden. Because optimal clearance required TNF-alpha after the onset of infection, we hypothesized that it may regulate T cell function. Lung CD3+ cells were the dominant population of TNF-alpha-producing cells (approximately 40%-70%). Neutralization of this cytokine decreased the number of memory T cells but not the number of activated, proliferating, or interferon-gamma-producing cells. T cells from infected, TNF-alpha-neutralized mice failed to protect T cell-deficient mice. The absence of TNF-alpha induces a defect in T cell-mediated protection.

Adoptive Transfer↗
PubMed2006

Pulmonary V beta 4+ T cells from Histoplasma capsulatum-infected mice respond to a homologue of Sec31 that confers a protective response.

The population of V beta 4+ T cells expands in the lungs of C57BL/6 mice infected with Histoplasma capsulatum, and the elimination of these cells impairs protective immunity. To determine the antigen or antigens that trigger their proliferation, V beta 4+ T cell hybridomas were generated from the lungs and spleens of infected mice. We mapped the antigenic determinants by T cell Western blot. Pulmonary and splenic T cells recognized 3 regions comprising <25, 55-70, and 125-140 kDa. The majority of hybridomas from lungs, but not from spleens, responded to the high molecular mass region. A protein from that area was identified, by amino acid sequencing, as a homologue of Sec31 from Saccharomyces cerevisiae. Vaccination with recombinant Sec31 reduced fungal burden and improved survival in mice, and its efficacy was critically dependent on the presence of V beta 4+ T cells. Thus, a homologue of Sec31 is a trigger of the expansion of the V beta 4+ T cell population and is important to the generation of protective immunity.

Animals↗
PubMed1997

Cross-reactivity in Histoplasma capsulatum variety capsulatum antigen assays of urine samples from patients with endemic mycoses.

We evaluated cross-reactivity in the antigen assay used for the diagnosis of histoplasmosis by testing urine samples from patients with disseminated fungal infections. The mycoses chosen for this study were selected on the basis of the observation that during clinical testing, cross-reactions may occur between Histoplasma capsulatum var. capsulatum, Paracoccidioides brasiliensis, Blastomyces dermatitidis, Coccidioides immitis, and Penicillium marneffei. We detected antigen in 12 of 19 patients with blastomycosis, 8 of 9 with paracoccidioidomycois, in 17 of 18 with P. marneffei infection, and in one with disseminated H. capsulatum var. duboisii infection. Cross-reactions were not observed in the assays for six patients with disseminated coccidioidomycosis. Cross-reactivity between the agents of other endemic mycoses should be considered in interpreting a positive H. capsulatum var. capsulatum antigen assay. Antigen detection may provide a rapid, provisional diagnosis for patients with serious infections caused by one of these organisms.

Antigens, Fungal↗
PubMed1997

Alterations to the cell wall of Histoplasma capsulatum yeasts during infection of macrophages or epithelial cells.

Many Histoplasma capsulatum strains have alpha-(1,3)-glucan in their cell walls and spontaneously produce variants that lack this polymer. The variants, in contrast to the parents, exist in aberrant shapes within macrophages. Here, the ultrastructure of the parental and variant cell walls was examined. All yeasts had identical electron-lucent, thick walls when grown in broth culture. However, ingestion by either macrophages or hamster trachea epithelial (HTE) cells caused the walls of variants to become electron-dense, thin, and sinuous. Parental strains remained unchanged in macrophages. Within HTE cells inoculated with parental strains, some organisms retained a thick wall and alpha-(1,3)-glucan but appeared to be degrading. In contrast, apparently intact intracellular yeasts had thin, wavy walls lacking alpha-(1,3)-glucan. A microenvironment within HTE cells that is unfavorable for the parental phenotype may trigger this ultrastructural change, potentially explaining why only variant yeasts are harvested from such cultures.

Animals↗
PubMed2003

Identifying phase-specific genes in the fungal pathogen Histoplasma capsulatum using a genomic shotgun microarray.

A fundamental feature of the fungal pathogen Histoplasma capsulatum is its ability to shift from a mycelial phase in the soil to a yeast phase in its human host. Each form plays a critical role in infection and disease, but little is understood about how these two morphologic phases are established and maintained. To identify phase-regulated genes of H. capsulatum, we carried out expression analyses by using a genomic shotgun microarray representing approximately one-third of the genome, and identified 500 clones that were differentially expressed. Genes induced in the mycelial phase included several involved in conidiation, cell polarity, and melanin production in other organisms. Genes induced in the yeast phase included several involved in sulfur metabolism, extending previous observations that sulfur metabolism influences morphology in H. capsulatum. Other genes with increased expression in the yeast phase were implicated in nutrient acquisition and cell cycle regulation. Unexpectedly, differential regulation of the site of transcript initiation was also observed in the two phases. These findings identify genes that may determine some of the major characteristics of the mycelial and yeast phases.

Blotting, Northern↗
PubMed2005

Identification of Histoplasma capsulatum transcripts induced in response to reactive nitrogen species.

The pathogenic fungus Histoplasma capsulatum escapes innate immune defenses and colonizes host macrophages during infection. After the onset of adaptive immunity, the production of the antimicrobial effector nitric oxide (*NO) restricts H. capsulatum replication. However, H. capsulatum can establish persistent infections, indicating that it survives in the host despite exposure to reactive nitrogen species (RNS). To understand how H. capsulatum responds to RNS, we determined the transcriptional profile of H. capsulatum to *NO-generating compounds using a shotgun genomic microarray. We identified 695 microarray clones that were induced > or = 4-fold upon nitrosative stress. Because our microarray clones were generated from random fragments of genomic DNA, they did not necessarily correspond to H. capsulatum open reading frames. To identify induced genes, we used high-density oligonucleotide tiling arrays to determine the genomic boundaries and coding strand of 153 RNS-induced transcripts. Homologues of these genes in other organisms are involved in iron acquisition, energy production, stress response, protein folding/degradation, DNA repair, and *NO detoxification. Ectopic expression of one of these genes, a P450 nitric oxide reductase homologue, was sufficient to increase resistance of H. capsulatum to RNS in culture. We propose that H. capsulatum uses the pathways identified here to cope with RNS-induced damage during pathogenesis.

Alkenes↗