Cryptococcus neoformans
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ABSTRACT:
PROVIDER: PRJNA192974 | ENA |
REPOSITORIES: ENA
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Project description:Virulence of Cryptococcus neoformans for mammals was proposed to emerge from evolutionary pressures on its natural environment by protozoan predators, which selected for strategies that allow survival within macrophages. In fact, Acanthamoeba castellanii ingests yeast cells, which then replicate intracellularly. In addition, most fungal factors needed to establish infection in the mammalian host are also important for survival within the amoeba. To better understand the origin of C. neoformans virulence, we compared the transcriptional profile of yeast cells internalized by amoebae and murine macrophages after 6 h of infection. Our results showed 656 and 293 genes whose expression changed at least two-fold in response to the intracellular environments of amoebae and macrophages, respectively. Among the genes common to both groups, we focused on the ORF CNAG_05662, which was potentially related to sugar transport. We constructed a mutant strain and evaluated its ability to grow on various carbon sources. The results showed that this gene, named PTP1 (Polyol Transporter Protein 1), is involved in the transport of 5- and 6-carbon polyols but its absence had no effect on virulence. Overall, our results are consistent with the hypothesis that mammalian virulence originated from fungal-protozoal interactions and provide a better understanding of how C. neoformans adapts to the mammalian host.
2013-03-14 | GSE45027 | GEO
Project description:Virulence of Cryptococcus neoformans for mammals was proposed to emerge from evolutionary pressures on its natural environment by protozoan predators, which selected for strategies that allow survival within macrophages. In fact, Acanthamoeba castellanii ingests yeast cells, which then replicate intracellularly. In addition, most fungal factors needed to establish infection in the mammalian host are also important for survival within the amoeba. To better understand the origin of C. neoformans virulence, we compared the transcriptional profile of yeast cells internalized by amoebae and murine macrophages after 6 h of infection. Our results showed 656 and 293 genes whose expression changed at least two-fold in response to the intracellular environments of amoebae and macrophages, respectively. Among the genes common to both groups, we focused on the ORF CNAG_05662, which was potentially related to sugar transport. We constructed a mutant strain and evaluated its ability to grow on various carbon sources. The results showed that this gene, named PTP1 (Polyol Transporter Protein 1), is involved in the transport of 5- and 6-carbon polyols but its absence had no effect on virulence. Overall, our results are consistent with the hypothesis that mammalian virulence originated from fungal-protozoal interactions and provide a better understanding of how C. neoformans adapts to the mammalian host. Four conditions, pairwise-compared: cells in vegetative growth at 28C versus cells within amoebae at 28C; and cells in vegetative growth at 37C/5% CO2 versus cells within macrophages at 37C/5% CO2. Three biological replicates for each condition. One replicate per array.
2013-03-14 | E-GEOD-45027 | biostudies-arrayexpress
Project description:Cryptococcus neoformans interactions with murine macrophages are critical for disease. In this project we analyzed fungal proteins which were co-purified with murine host proteins after interaction. H99 C. neoformans was opsonized with mAb 18B7 and addedd to murine macrophages. Then murine cells were lysed and cell extracts submitted to proteomics.
2023-03-11 | PXD024951 | Pride
Project description:We measured protein translation (by ribosome profiling) and RNA levels (by polyA-enriched RNA-seq) in Cryptococcus neoformans strain H99 and Cryptococcus neoformans strain JEC21. This is the first transcriptome-wide map of translation in this species complex.
2019-06-22 | GSE133125 | GEO
Project description:We examined four subsets of alveolar macrophages differentiated by CXCL2 expression and FLT3 fate mapping induced by Cryptococcus neoformans infection. These four subpopulations have distinct mRNA expression pattern indicating the heterogenity within alveolar macrophages.
2020-06-08 | GSE133026 | GEO
Project description:We examined two subpopulations of alveolar macrophages differentiated by CXCL2 expression stimulated by Cryptococcus neoformans. The two subpopulations have distinct mRNA expression pattern indicating the heterogenity within alveolar macrophages.
2020-06-08 | GSE146234 | GEO
Project description:Cryptococcus neoformans is a human fungal pathogen found ubiquitously within the environment and associated with infection of primarily immunocompromised individuals. Without the activation of an effective immune response, the pathogen can survive, proliferate, and disseminate throughout the host through the action of diverse virulence factors. These virulence factors include a polysaccharide capsule to protect the fungus from phagocytosis by macrophages, melanin production to neutralize reactive oxygen species, thermotolerance to survive at human physiological temperatures, and extracellular enzymes for host tissue degradation and invasion. We previously used mass spectrometry-based proteomics to explore the production of fungal virulence factors during infection using in vitro (macrophages) and in vivo (murine) models of disease. Based on our studies, we investigated the proteome response of C. neoformans upon disruption of CipC, a virulence-associated fungal protein.
2024-10-13 | PXD056761 | Pride
Project description:We investigated the effects of the hypoxia-mimetic CoCl2 on the gene expression of pathogenic fungus Cryptococcus neoformans. Keywords: compound treatment design
2009-05-01 | GSE11390 | GEO
Project description:Human infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
2014-12-31 | GSE57720 | GEO
Project description:Thermotolerance, a key factor essential for the virulence of pathogenic fungi including Cryptococcus neoformans, remains largely unexplored in terms of its underlying mechanism. In this study, our findings demonstrate that Set3C, a widely distributed and conserved histone deacetylase complex, is required for thermotolerance in Cryptococcus neoformans. Specifically, the deletion of the core subunit Set302, responsible for the integrity of the complex, results in a significant reduction in the growth ability under high stress and the viability at extreme temperature. Moreover, the absence of Set302 leads to a decrease in the production of capsule and melanin. Transcriptomics analysis revealed that Set302 regulates a large number of genes compared to normal condition, and their expression is responsive to heat stress. Notably, we observed that Set302 positively influences the expression of genes related to ubiquitin-proteasome system (UPS) at high temperature. Using GFP-α-synuclein overexpression model, we observed a pronounced accumulation of misfolded proteins under heat stress, consequently inhibiting the thermotolerance of Cryptococcus neoformans. Furthermore, the loss of Set302 exacerbates this inhibition of thermotolerance. Interestingly, set302∆ strain exhibits a similar phenotype under proteasome stress as it does under high temperature. We also found that set302∆ strain displayed significantly reduced pathogenicity and colonization ability compared to the wild-type strain in the murine infection model. Collectively, our findings indicate that Set302 modulates the degradation of misfolded proteins through the UPS pathway, thereby affecting the thermotolerance and pathogenicity of Cryptococcus neoformans.
2023-09-05 | GSE242109 | GEO