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PubMedDate not supplied

Role of cytokines in T cell immunity to a pulmonary Cryptococcus neoformans infection.

The objective of these studies was to present an overview of our studies of the cytokine network and cellular interactions responsible for the T-cell-mediated inflammatory response in the lungs following infection by Cryptococcus neoformans. In a resistant strain of mice, moderately virulent cryptococci were progressively cleared from the lungs after week 1. Characterization of mitogen-induced cytokine production demonstrated that the T cells in the lungs during the first 3 weeks of infection resembled Th0 rather than Th1 cells. In addition, the production of IL-10 (by mitogen-stimulated leukocytes) could promote an increase in the ratio of Th2:Th1 cytokines in short-term in vitro cultures. In vivo, there were increases in the alveolar levels of tumor necrosis factor-alpha and IL-6 at weeks 1-3 and the chemokines monocyte chemoattractant protein-1 at weeks 1-2 followed by macrophage inflammatory protein-1 alpha and ENA-78 at week 3. Overall, the pulmonary inflammatory response to C. neoformans evolved over 5 weeks from granulocytic to mononuclear, suggesting a maturation to a Th1-type response by week 5.

Animals↗
PubMed1990

Gastrointestinal, hepatic, and pancreatic involvement with Cryptococcus neoformans in AIDS.

We describe three cases of acquired immunodeficiency syndrome (AIDS) complicated by disseminated cryptococcosis with gastrointestinal involvement. The stomach, duodenum, colon, pancreas, and liver showed invasion by the fungus. Although none of the patients had any symptoms attributable to Cryptococcus neoformans, we speculate that cryptococcal invasion of the liver and gastrointestinal tract may be a contributor to the morbidity in these immunocompromised patients.

Acquired Immunodeficiency Syndrome↗
PubMed1997

IL-18 protects mice against pulmonary and disseminated infection with Cryptococcus neoformans by inducing IFN-gamma production.

We examined the effects of a newly identified cytokine, IL-18, originally designated as IFN-gamma-inducing factor, in a mouse model of pulmonary and disseminated infection with a highly virulent strain of Cryptococcus neoformans. Administration of murine rIL-18 enhanced elimination of live micro-organisms from the lungs, prevented fungal dissemination to the brain, reduced the level of serum cryptococcal capsular polysaccharide Ags, and increased the survival rate of infected mice. Histologic examination of lung sections of infected and PBS-treated mice showed a poor cellular inflammatory reaction and a large number of multiplying C. neoformans yeast cells in alveolar spaces. In contrast, massive infiltration of inflammatory cells, consisting mainly of mononuclear cells, characterized sections of lungs of infected animals treated with IL-18. Treatment with IL-18 also increased the level of serum IFN-gamma. In addition, the protective effect of IL-18 on cryptococcal infection was abrogated by administration of neutralizing anti-IFN-gamma mAb. Finally, we examined the effect of neutralizing anti-IL-18 Ab on cryptococcal infection to define the physiologic role of this cytokine in host defense using another weakly virulent strain of C. neoformans, which induced the expression of IL-18 mRNA in the infected lungs. Administration of this Ab exacerbated the infection, as shown by the increased lung burden. Our results indicate that IL-18 plays an important role in host defense against infection with C. neoformans.

Animals↗
PubMed1999

Topoisomerase I is essential in Cryptococcus neoformans: role In pathobiology and as an antifungal target.

Topisomerase I is the target of several toxins and chemotherapy agents, and the enzyme is essential for viability in some organisms, including mice and drosophila. We have cloned the TOP1 gene encoding topoisomerase I from the opportunistic fungal pathogen Cryptococcus neoformans. The C. neoformans topoisomerase I contains a fungal insert also found in topoisomerase I from Candida albicans and Saccharomyces cerevisiae that is not present in the mammalian enzyme. We were unable to disrupt the topoisomerase I gene in this haploid organism by homologous recombination in over 8000 transformants analyzed. When a second functional copy of the TOP1 gene was introduced into the genome, the topoisomerase I gene could be readily disrupted by homologous recombination (at 7% efficiency). Thus, topoisomerase I is essential in C. neoformans. This new molecular strategy with C. neoformans may also be useful in identifying essential genes in other pathogenic fungi. To address the physiological and pathobiological functions of the enzyme, the TOP1 gene was fused to the GAL7 gene promoter. The resulting GAL7::TOP1 fusion gene was modestly regulated by carbon source in a serotype A strain of C. neoformans. Modest overexpression of topoisomerase I conferred sensitivity to heat shock, gamma-rays, and camptothecin. In contrast, alterations in topoisomerase I levels had no effect on the toxicity of a novel class of antifungal agents, the dicationic aromatic compounds (DACs), indicating that topoisomerase I is not the target of DACs. In an animal model of cryptococcal meningitis, topoisomerase I regulation was not critically important to established infection, but may impact on the initial stress response to infection. In summary, our studies reveal that topoisomerase I is essential in the human pathogen C. neoformans and represents a novel target for antifungal agents.

Amino Acid Sequence↗
PubMed1991

[Pulmonary pseudotumor caused by Cryptococcus neoformans].

Since 1923, eight cases of cryptococcosis have been described in Norway, all with meningeal affection. A distinct, solitary infiltration in the upper lobe of the right lung was discovered in a 68 year-old woman. The lobe was extirpated. Microbiological and histological investigations showed infection with Cryptococcus neoformans. No antimycotic treatment was given. Four months later the patient developed osteomyelitis of the skull due to cryptococcosis, and was treated successfully with amphotericin B and flucytosin. Further investigation of the patient revealed a defect in the T-lymphocyte immune system, but it is uncertain whether this was of any significance for the development of the cryptococcus infection.

Aged↗
PubMed1987

Oral Cryptococcus neoformans infection in AIDS.

Opportunistic fungal and parasitic infections account for a significant amount of the morbidity and the mortality associated with the acquired immune deficiency syndrome (AIDS). Oral fungal infections are limited primarily to Candida albicans. The first reported case of oral Cryptococcus neoformans infection in a patient with AIDS is presented.

Acquired Immunodeficiency Syndrome↗
PubMed2026

Distinct STRIPAK subunits drive conserved and subunit-specific signaling programs in Cryptococcus neoformans.

The striatin-interacting phosphatase and kinase (STRIPAK) complex is a conserved PP2A-associated signaling hub that integrates kinase-phosphatase networks, yet its roles in human fungal pathogens remain poorly defined. Here, we dissected STRIPAK functions in the opportunistic pathogen Cryptococcus neoformans by combining genetic, genomic, virulence, and phosphoproteomic analyses across mutants lacking individual STRIPAK subunits. Loss of the core STRIPAK components via PPH22, FAR8, FAR9, or FAR11 mutations caused severe defects in growth, stress adaptation, cell-cycle progression, and morphogenesis, accompanied by widespread aneuploidy and genome instability. In murine infection models, far11Δ strains were avirulent, whereas far9Δ mutants caused delayed but ultimately fatal disease and underwent host-associated genome remodeling, with recovered isolates exhibiting chromosome 11 amplification despite no consistent in vitro fitness advantage. In contrast, deletion of MOB3 produced a hypervirulent phenotype. mob3Δ cells exhibited enhanced transmigration across an in vitro blood-brain barrier model, increased survival in macrophages, and generated small-cell morphotypes, features associated with increased dissemination. Phosphoproteomic profiling revealed extensive and overlapping phosphorylation changes among core STRIPAK mutants, affecting pathways involved in signaling, cytoskeletal and cell-cycle control, chromatin regulation, RNA metabolism, and stress responses. Conversely, mob3Δ mutants displayed a smaller, largely distinct phosphoproteomic signature. Network and functional enrichment analyses highlighted STRIPAK-dependent regulation of TORC2-associated signaling, MAPK/GTPase signaling, autophagy, nuclear transport, RNA processing, DNA replication, and ribosome biogenesis. Together, these findings establish STRIPAK as a coordinator of genome stability, morphological plasticity, stress adaptation, and virulence in C. neoformans, and demonstrate that individual STRIPAK subunits drive shared yet divergent signaling outputs that shape host-pathogen interactions.

Journal Article↗
PubMed2000

[In vitro activity of a liposomal nystatin formulation (Nyotran) against Cryptococcus neoformans].

The in vitro antifungal activity of a new liposomal nystatin formulation (NISTL, Nyotran, Aronex Ltd., EE.UU.) was evaluated by a microdilution method with RPMI based on the M27A document of the National Committee for Clinical Laboratory Standards (NCCLS) against 22 isolates of Cryptococcus neoformans. This antifungal activity was compared with those of other seven antifungal agents, such as nystatin (NIST), amphotericin B deoxycholate, liposomal amphotericin B, amphotericin B lipid complex, amphotericin B colloidal dispersion, fluconazole, and itraconazole. NISTL was more active in vitrothan NIST, showing MIC values 2-3 fold smaller in 90% of the isolates. The results obtained suggest that this new formulation would be very helpful for the treatment of cryptococcosis.

English Abstract↗
PubMed1992

Coulter counter identifies Cryptococcus neoformans as leukocytes. A case of pseudopleocytosis.

Cerebrospinal fluid from a 42-year-old man with acquired immune deficiency syndrome was processed in a Coulter S-plus counter and found to contain "4.8 x 10(9) leukocytes/L:56.1% granulocytes and 37.7% lymphocytes." Direct examination of the same specimen in a counting chamber revealed that the leukocytes were cells of Cryptococcus neoformans. Coulter analysis of cerebrospinal fluid may be inappropriate, particularly when yeast infection is a probable diagnosis.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Assessment of Difco ESP 384 blood culture system by terminal subcultures: failure to detect Cryptococcus neoformans in clinical specimens.

Terminal subcultures were performed on 1,162 5-day negative blood culture sets which had been monitored by the Difco ESP 384, a continuous-monitor blood culture system. Of these, 16 (1.4%) had growth upon terminal subculture. The isolates not detected by the Difco ESP 384 were Cryptococcus neoformans (eight isolates), Candida albicans (one isolate), Staphylococcus aureus (two isolates) coagulase-negative staphylococcus (three isolates), Bacillus sp. (one isolate), and Corynebacterium sp. (one isolate). Acridine orange staining was performed on 200 randomly selected negative blood culture sets from the study group. Of these, two sets were positive and grew out C. neoformans, as did the terminal subculture. A review of patient's medical records indicated that many of these false-negative isolates were clinically insignificant. The Difco ESP 384 failed to detect 1.4% of the isolates in this study, 50% of which were C. neoformans, indicating a deficiency in the detection mechanism of the system. Further studies demonstrated that while these isolates (C. neoformans) grew in the Difco media, the system did not detect this growth when the standard 5-day protocol was used.

Cryptococcosis↗
PubMed1991

T cell-mediated immunity in the lung: a Cryptococcus neoformans pulmonary infection model using SCID and athymic nude mice.

T cells are important in systemic anticryptococcal defenses, but a role in controlling an initial pulmonary infection has not been demonstrated. A murine model with intratracheal inoculation was developed to study the acquisition and expression of pulmonary T cell-mediated immunity against Cryptococcus neoformans. Infections with four strains of C. neoformans (305, 68A, 613D, and 52D) in two strains of mice (BALB/c and C57BL/6) were examined. Unencapsulated strain 305 and slowly growing strain 68A were readily controlled apparently by nonimmune pulmonary defenses, and no extrapulmonary dissemination was detected. Strain 613D grew progressively in the lungs and disseminated to the brain and spleen. Strain 52D initially grew rapidly in the lungs and disseminated to the spleen, but a clearance mechanism developed in the lungs after day 7 postinfection and in the spleen after day 28. SCID and athymic nude mice were unable to clear a strain 52D pulmonary infection, and a lethal disseminated infection occurred. Pulmonary clearance could be adoptively transferred into SCID mice infected with strain 52D by use of immune T cells from the spleen and lungs and hilar lymph nodes of infected immunocompetent donors. Furthermore, pulmonary clearance was almost 100-fold better in SCID mice that received immune T cells from the lungs and hilar lymph nodes than in those that received immune T cells from the spleen, even though equivalent levels of delayed-type hypersensitivity were transferred by both cell populations. These adoptive transfer studies suggested that the lung and hilar lymph node T cells from immune animals either are enriched in such a way as to mediate protective immunity or home to the lungs better than do splenic T cells.

Animals↗
PubMed1998

Risk factors in necrotizing fasciitis: a case involving Cryptococcus neoformans.

Necrotizing fasciitis is a destructive soft tissue infection that is most typically caused by group A streptococci or a combination of facultative and anaerobic bacteria. Patients at risk for the development of necrotizing fasciitis often have compromised immune function or poor tissue perfusion. This report describes a case of necrotizing fasciitis caused by Cryptococcus neoformans, a pathogen not previously associated with this primary destructive soft tissue infection. The process occurred in a patient at risk for the development of opportunistic infection. We briefly review the risk factors for the development of necrotizing fasciitis and the typical bacteriologic findings. Cryptococcal infections and their treatment are described. Despite the uncommon pathogen, the treatment of this patient followed established principles-prompt surgical intervention and systemic antimicrobial therapy tailored to the offending organisms.

Adult↗
PubMed1985

Cholangitis associated with Cryptococcus neoformans.

A 15-yr-old girl presented with complaints of right upper quadrant pain and jaundice. Elevation of serum alkaline phosphatase, signs of protal hypertension, and computed tomographic scan findings suggested a diagnosis of primary sclerosing cholangitis. However, cultures of the bile and of the common bile duct specimen obtained during a surgical procedure grew Cryptococcus neoformans. Treatment with amphotericin B was begun. An episode of upper gastrointestinal bleeding, however, led to the hepatorenal syndrome, and the patient died before antifungal therapy was completed. At autopsy, active sclerosing cholangitis associated with cryptococci involved the common bile duct. We suggest that opportunistic infection of the biliary tree should be considered in pediatric patients with presumed primary sclerosing cholangitis.

Adolescent↗