Candida albicans
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ABSTRACT:
PROVIDER: PRJNA326692 | ENA |
REPOSITORIES: ENA
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Project description:The opportunistic fungal pathogen Candida albicans is a common cause of life-threatening nosocomial bloodstream infections. In the murine model of systemic candidiasis the kidney is the primary target organ while the fungal load declines over time in liver and spleen. To get a better understanding of the organ-specific differences in host-pathogen interaction during systemic murine candidiasis, we performed a time-course gene expression profiling to investigate the differential responses of murine kidney, liver and spleen and determined the fungal transcriptome in liver and kidney. We clearly demonstrate a delayed immune response on the transcriptional level in kidney accompanied by late induction of fungal stress response genes in this organ. In contrast, early upregulation of the proinflammatory response in the liver was associated with a fungal transcriptional profile resembling that of phagocytosed cells, suggesting that the resident phagocytic system contributes significantly to fungal control in the liver. Although no visible filamentation occurred in the liver, C. albicans hypha-associated genes were upregulated, indicating an uncoupling of gene expression and morphology during infection of this organ. In vitro the induction of hypha-associated gene expression in yeast cells led to altered interaction with macrophages, suggesting that the observed transcriptional changes affect host-pathogen interaction in vivo. Consistently, the combination of host and pathogen transcriptional data in an inference network model implied that C. albicans cell wall remodeling and metabolism were connected to the immune responses in kidney and liver. Furthermore, the network suggested links between fungal iron acquisition and amino acid metabolism in the kidney and host organ homeostasis. Thus, this work provides novel insights into the organ-specific host-pathogen interactions during systemic C. albicans infection.
2016-11-18 | GSE83679 | GEO
Project description:Combined transcriptional profiling during systemic candidiasis reveals organ-specific host-pathogen interactions
| PRJNA326689 | ENA
Project description:The opportunistic fungal pathogen Candida albicans is a common cause of life-threatening nosocomial bloodstream infections. In the murine model of systemic candidiasis the kidney is the primary target organ while the fungal load declines over time in liver and spleen. To get a better understanding of the organ-specific differences in host-pathogen interaction during systemic murine candidiasis, we performed a time-course gene expression profiling to investigate the differential responses of murine kidney, liver and spleen and determined the fungal transcriptome in liver and kidney. We clearly demonstrate a delayed immune response on the transcriptional level in kidney accompanied by late induction of fungal stress response genes in this organ. In contrast, early upregulation of the proinflammatory response in the liver was associated with a fungal transcriptional profile resembling that of phagocytosed cells, suggesting that the resident phagocytic system contributes significantly to fungal control in the liver. Although no visible filamentation occurred in the liver, C. albicans hypha-associated genes were upregulated, indicating an uncoupling of gene expression and morphology during infection of this organ. In vitro the induction of hypha-associated gene expression in yeast cells led to altered interaction with macrophages, suggesting that the observed transcriptional changes affect host-pathogen interaction in vivo. Consistently, the combination of host and pathogen transcriptional data in an inference network model implied that C. albicans cell wall remodeling and metabolism were connected to the immune responses in kidney and liver. Furthermore, the network suggested links between fungal iron acquisition and amino acid metabolism in the kidney and host organ homeostasis. Thus, this work provides novel insights into the organ-specific host-pathogen interactions during systemic C. albicans infection.
2016-11-18 | GSE83681 | GEO
Project description:The opportunistic fungal pathogen Candida albicans is a common cause of life-threatening nosocomial bloodstream infections. In the murine model of systemic candidiasis the kidney is the primary target organ while the fungal load declines over time in liver and spleen. To get a better understanding of the organ-specific differences in host-pathogen interaction during systemic murine candidiasis, we performed a time-course gene expression profiling to investigate the differential responses of murine kidney, liver and spleen and determined the fungal transcriptome in liver and kidney. We clearly demonstrate a delayed immune response on the transcriptional level in kidney accompanied by late induction of fungal stress response genes in this organ. In contrast, early upregulation of the proinflammatory response in the liver was associated with a fungal transcriptional profile resembling that of phagocytosed cells, suggesting that the resident phagocytic system contributes significantly to fungal control in the liver. Although no visible filamentation occurred in the liver, C. albicans hypha-associated genes were upregulated, indicating an uncoupling of gene expression and morphology during infection of this organ. In vitro the induction of hypha-associated gene expression in yeast cells led to altered interaction with macrophages, suggesting that the observed transcriptional changes affect host-pathogen interaction in vivo. Consistently, the combination of host and pathogen transcriptional data in an inference network model implied that C. albicans cell wall remodeling and metabolism were connected to the immune responses in kidney and liver. Furthermore, the network suggested links between fungal iron acquisition and amino acid metabolism in the kidney and host organ homeostasis. Thus, this work provides novel insights into the organ-specific host-pathogen interactions during systemic C. albicans infection.
2016-11-18 | GSE83680 | GEO
Project description:Candida albicans is exposed to a different host environment during different site of infection. Thus, different virulence factors may be active during differenttypes of infection. However,little is known about the C. albicans genes that are required for the initiation and maintenance of candidiasis. To identify potential virulence factors relevant to hematogenously disseminated candidiasis, we determined the transcriptional response of C. albicans to human umbilical vein endothelial cells (HUVECs) in vitro. Keywords: cell interaction
2008-12-01 | GSE5344 | GEO
Project description:Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections. However, human antifungal immunity remains poorly defined. By integrating transcriptional analysis and functional genomics we identified Candida-specific host defense mechanisms in humans. Candida induced significant (p<10-35) expression of genes from the type I interferon (IFN) pathway in human peripheral blood mononuclear cells. This unexpectedly prominent role of type I IFN pathway in anti-Candida host defense was supported by additional evidence. Polymorphisms in type I IFN genes modulated Candida-induced cytokine production and were correlated with susceptibility to systemic candidiasis. In in-vitro experiments, type I IFNs skewed Candida-induced inflammation from a Th17-response toward a Th1-response. Patients with chronic mucocutaneaous candidiasis displayed defective expression of genes in the type I IFN pathway. These findings indicate that the type I IFN pathway is a main signature of Candida-induced inflammation and plays a crucial role in anti-Candida host defense in humans.
2012-12-01 | GSE42630 | GEO
Project description:Candida albicans is the most common human fungal pathogen causing mucosal and systemic infections. However, human antifungal immunity remains poorly defined. By integrating transcriptional analysis and functional genomics we identified Candida-specific host defense mechanisms in humans. Candida induced significant (p<10-35) expression of genes from the type I interferon (IFN) pathway in human peripheral blood mononuclear cells. This unexpectedly prominent role of type I IFN pathway in anti-Candida host defense was supported by additional evidence. Polymorphisms in type I IFN genes modulated Candida-induced cytokine production and were correlated with susceptibility to systemic candidiasis. In in-vitro experiments, type I IFNs skewed Candida-induced inflammation from a Th17-response toward a Th1-response. Patients with chronic mucocutaneaous candidiasis displayed defective expression of genes in the type I IFN pathway. These findings indicate that the type I IFN pathway is a main signature of Candida-induced inflammation and plays a crucial role in anti-Candida host defense in humans. 3 healthy controls and 2 CMC patients
2012-12-01 | E-GEOD-42630 | biostudies-arrayexpress
Project description:Candida albicans is exposed to a different host environment during oropharyngeal candidiasis (OPC) compared to hematogenously disseminated candidiasis. Thus, different virulence factors may be active during these two types of infection. However,little is known about the C. albicans genes that are required for the initiation and maintenance of OPC. To identify potential virulence factors relevant to this disease, we determined the transcriptional response of C. albicans to oral epithelial cells in vitro. Keywords: cell interaction
2008-12-01 | GSE5340 | GEO
Project description:Candida albicans is a commensal of the urogenital tract and the predominant cause of vulvovaginal candidiasis (VVC). Roughly, 70% of otherwise healthy women succumb to VVC at least once in their life time. Elevated oestrogen levels are associated with C. albicans colonisation of the vagina and symptomatic infection. However, little is known about how C. albicans adapts to oestrogen. Here, we investigate how adaptation of C. albicans to elevated concentrations of oestrogen on the C. albicans host-pathogen interaction. Growth of C. albicans in physiological relevant concentrations of oestrogen promoted fungal innate immune evasion through reduction of both macrophage and neutrophil phagocytosis. Oestrogen-induced innate immune evasion was mediated via inhibition of opsonophagocytosis through enhanced Gpd2 dependent acquisition of Factor H on the fungal cell surface. The zebrafish larval model of infection confirmed that in vivo oestrogen and Gpd2 promote pathogenicity. Understanding the impact of oestrogen on C. albicans host-pathogen interaction will help improve our knowledge on how oestrogen promotes VVC.
2022-01-04 | GSE145240 | GEO
Project description:Candida albicans is exposed to a different host environment during different site of infection. Thus, different virulence factors may be active during differenttypes of infection. However,little is known about the C. albicans genes that are required for the initiation and maintenance of candidiasis. To identify potential virulence factors relevant to hematogenously disseminated candidiasis, we determined the transcriptional response of C. albicans to human umbilical vein endothelial cells (HUVECs) in vitro. Keywords: cell interaction Two different Candida albicans strains, CAI4-URA and a clinical isolate 36082, were used to identify the transcriptional response of C. albicans to HUVECs. The strains were incubated with either the HUVECs or bare plastic for 45, 90, and 180 min. C. albicans RNA was extracted and the transcriptional profile of these organisms was analyzed using the C. albicans oligonucleotide microarray. The transcriptional response to HUVECs was compared to that to bare plastic as a control condition. Each time point contains six biological replicates, three of which are from each C. albicans strain.
2010-06-30 | E-GEOD-5344 | biostudies-arrayexpress