E-MTAB-5134
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ABSTRACT:
PROVIDER: E-MTAB-5134 | ExpressionAtlas | 2016-10-24
REPOSITORIES: ExpressionAtlas
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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 | 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: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:We addressed the question how the interaction between the beneficial root endophyte Serendipita vermifera (Sv) and the pathogen Bipolaris sorokiniana (Bs) affects fungal behavior and determines barley host responses using a gnotobiotic natural soil-based split-root system for phenotypic and transcriptional analyses.
2019-07-06 | GSE130517 | GEO
Project description:a de novo transcriptomic analysis to reveal key virulence factors of the aphid pathogen C. obscurus. The transcript levels of the related genes in the samples of in vitro fungal culture and mycotized cadavers were analyzed
2019-08-20 | GSE105072 | GEO
Project description:The kinase, putative endopeptidase and other peptides of small size (KEOPS) complex plays critical cellular functions in eukaryotes, but its pathobiological roles remains elusive in fungal pathogens. Here we comprehensively analyze the pathobiological functions of the KEOPS complex in fungal meningoencephalitis pathogen Cryptococcus neoformans. The cryptococcal KEOPS complex appears to have a linear arrangement of Pcc1-Kae1-Bud32-Cgi121, supported by physical interaction between Pcc1-Kae1, Kae1-Bud32, and Bud32-Cgi121, but does not have Gon7 ortholog, which is the part of the S. cerevisiae KEOPS complex. Deletion of PCC1, KAE1, and BUD32 causes severe growth defects with perturbed cell cycle control.
2022-10-18 | GSE208333 | GEO
Project description:The biotrophic fungal pathogen Ustilago maydis cause common smut in maize, and lead to gall formation on all aerial organs, especially on maize kernel thus reduce yield. The interaction of U. maydis with maize is a well-established model to study the interaction between maize and biotrophic pathogen. U. maydis infection could activate host immune responses including: ROS accumulation, protease activation, salicylic acid signaling. U. maydis employ several strategies to overcome maize immune response, thus initial the biotrophic interaction with host. It has been suggested that genetic factors of maize host affected the disease severity of U. maydis infection, here we investigated the transcriptome profile of resistance and susceptible maize lines upon U. maydis infection, thus propose candidate maize genes involved in the defense response in maize to corn smut cause by U. maydis.
2021-04-15 | GSE172071 | GEO
Project description:Transcriptome profiling to identify Cap2/Hap43 regulons in the human fungal pathogen Candida albicans: Wild type vs. cap2D grown in iron-depleted medium
2011-05-25 | GSE28429 | GEO