Host pathogen interaction at a transcriptional level
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ABSTRACT:
PROVIDER: PRJNA109763 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Host and pathogen interaction: time course
| PRJNA147451 | 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 | GSE83679 | 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 | 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:A genomic insight into how an insect pest responds to the infection of a fungal insect pathogen, such as Beauveria bassiana, is critical for alternative strategy of insect pest contol based on fungal insecticides but has not been well probed. Here we constructed three pairs of digital expression libraries (transcriptomes) of Plutella xylostella (global lepidopteran pest) larvae 24, 36 and 48 hours post treatment of infection (hptI) and control (hptC) to reveal the host response to B. bassiana infection at genomic level. The paired libraries comprised 2144, 3200 and 2967 differentially expressed genes (DEGs) of P. xylostella at 24, 36 and 48 hptI/hptC, respectively. These DEGs were enriched in various immune pathways activated by the fungal infection, such as the pathways of complement and coagulation cascades, protein digestion and absorption, and drug metabolism - cytochrome P450. We found that 24 hptI was critical either for the cuticular penetration of B. bassiana or for the initial activation of the host defense system. The host immune response peaked at 36 hptI so that multiple defense mechanisms were activated against the fungal entry into the host hemocoel. At 48 hptI, many host genes involved in immunity and metabolism were downregulated, suggesting a success of fungal localization in the host hemocoel by overcoming the host defense reaction. Finally, we revealed that several fungal pathways could play important roles in the host-pathogen interaction, such as antioxidant activity, peroxidase activity and proteolysis. Up to 1636 fungal genes were co-expressed at the three time points, and 116 of them encode putative secretion proteins. Our results provide a novel insight into the pathogen-insect interaction and help to probe molecular mechanisms involved in the control of P. xylostella by B. bassiana. Here we constructed three pairs of digital expression libraries (transcriptomes) of Plutella xylostella (global lepidopteran pest) larvae 24, 36 and 48 hours post treatment of infection (hptI) and control (hptC) to reveal the host response to B. bassiana infection at genomic level
2016-04-06 | E-GEOD-72383 | biostudies-arrayexpress
Project description:The interaction between fungal pathogen and host during infection is a complex and dynamic process. To resolve this, we chose the zebrafish model organism as the host to study C. albicans infection via systems biology approach. Transcriptome microarray data and histological analysis of surviving fish were sampled at different post-infection time points. The dynamic variations of significant genes expression profiles in C. albicans and zebrafish were concurrently analyzed by principal component analysis (PCA). The PCA results clearly indicated that the infection of C. albicans can be divided into three phases that include adhesion, invasion and damage phases. The results were highly consistent with subsequent histological analysis. Furthermore, we found the primary ontology function of genes with significant variations in both C. albicans and zebrafish is iron related. Most of the iron related genes in C. albicans were over-expressed in late stage, while most of the iron related genes in zebrafish were suppressed at the same phase of infection. It suggested that the iron homeostasis function of the host was shut-down when massive hemorrhage in zebrafish occurred during later stages of infection. At the same time, the iron scavenging function of C. albicans was activated. This implied the competition for iron is an important issue between the host and the fungal pathogen during infection. When we administered excess iron into the microenvironment of infection site, the infection process was significantly delayed. That indicated the virulence of C. albicans is correlated with its protein-bond iron scavenging strategies. Our finings not only provided dynamic mechanistic views of the iron competition but also highlighted the potential regulatory schemes in fungal pathogenesis. Each fish was intraperitoneally injected with C. albicans cells and these infected fish were collected at 0.5, 1, 2, 4, 6, 8, 12, 16, 18 hpi. 0.625M-NM-<g of Cy3 cRNA for C. albicans array and 1.65 M-NM-<g of Cy3 cRNA for zebrafish array was fragmented to an average size of about 50-100 nucleotides by incubation with fragmentation buffer at 60M-BM-0C for 30 minutes. Each time points contain three biological repeat. For C. albicans array, each biological repeat has two technical replicate.
2013-08-26 | E-GEOD-32118 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-09-01 | E-GEOD-13405 | biostudies-arrayexpress
Project description:The interaction between fungal pathogen and host during infection is a complex and dynamic process. To resolve this, we chose the zebrafish model organism as the host to study C. albicans infection via systems biology approach. Transcriptome microarray data and histological analysis of surviving fish were sampled at different post-infection time points. The dynamic variations of significant genes expression profiles in C. albicans and zebrafish were concurrently analyzed by principal component analysis (PCA). The PCA results clearly indicated that the infection of C. albicans can be divided into three phases that include adhesion, invasion and damage phases. The results were highly consistent with subsequent histological analysis. Furthermore, we found the primary ontology function of genes with significant variations in both C. albicans and zebrafish is iron related. Most of the iron related genes in C. albicans were over-expressed in late stage, while most of the iron related genes in zebrafish were suppressed at the same phase of infection. It suggested that the iron homeostasis function of the host was shut-down when massive hemorrhage in zebrafish occurred during later stages of infection. At the same time, the iron scavenging function of C. albicans was activated. This implied the competition for iron is an important issue between the host and the fungal pathogen during infection. When we administered excess iron into the microenvironment of infection site, the infection process was significantly delayed. That indicated the virulence of C. albicans is correlated with its protein-bond iron scavenging strategies. Our finings not only provided dynamic mechanistic views of the iron competition but also highlighted the potential regulatory schemes in fungal pathogenesis.
2013-08-26 | GSE32118 | GEO
Project description:A genomic insight into how an insect pest responds to the infection of a fungal insect pathogen, such as Beauveria bassiana, is critical for alternative strategy of insect pest contol based on fungal insecticides but has not been well probed. Here we constructed three pairs of digital expression libraries (transcriptomes) of Plutella xylostella (global lepidopteran pest) larvae 24, 36 and 48 hours post treatment of infection (hptI) and control (hptC) to reveal the host response to B. bassiana infection at genomic level. The paired libraries comprised 2144, 3200 and 2967 differentially expressed genes (DEGs) of P. xylostella at 24, 36 and 48 hptI/hptC, respectively. These DEGs were enriched in various immune pathways activated by the fungal infection, such as the pathways of complement and coagulation cascades, protein digestion and absorption, and drug metabolism - cytochrome P450. We found that 24 hptI was critical either for the cuticular penetration of B. bassiana or for the initial activation of the host defense system. The host immune response peaked at 36 hptI so that multiple defense mechanisms were activated against the fungal entry into the host hemocoel. At 48 hptI, many host genes involved in immunity and metabolism were downregulated, suggesting a success of fungal localization in the host hemocoel by overcoming the host defense reaction. Finally, we revealed that several fungal pathways could play important roles in the host-pathogen interaction, such as antioxidant activity, peroxidase activity and proteolysis. Up to 1636 fungal genes were co-expressed at the three time points, and 116 of them encode putative secretion proteins. Our results provide a novel insight into the pathogen-insect interaction and help to probe molecular mechanisms involved in the control of P. xylostella by B. bassiana.
2016-04-06 | GSE72383 | GEO
Project description:The interaction between fungal pathogen and host during infection is a complex and dynamic process. To resolve this, we chose the zebrafish model organism as the host to study C. albicans infection via systems biology approach. Transcriptome microarray data and histological analysis of surviving fish were sampled at different post-infection time points. The dynamic variations of significant genes expression profiles in C. albicans and zebrafish were concurrently analyzed by principal component analysis (PCA). The PCA results clearly indicated that the infection of C. albicans can be divided into three phases that include adhesion, invasion and damage phases. The results were highly consistent with subsequent histological analysis. Furthermore, we found the primary ontology function of genes with significant variations in both C. albicans and zebrafish is iron related. Most of the iron related genes in C. albicans were over-expressed in late stage, while most of the iron related genes in zebrafish were suppressed at the same phase of infection. It suggested that the iron homeostasis function of the host was shut-down when massive hemorrhage in zebrafish occurred during later stages of infection. At the same time, the iron scavenging function of C. albicans was activated. This implied the competition for iron is an important issue between the host and the fungal pathogen during infection. When we administered excess iron into the microenvironment of infection site, the infection process was significantly delayed. That indicated the virulence of C. albicans is correlated with its protein-bond iron scavenging strategies. Our finings not only provided dynamic mechanistic views of the iron competition but also highlighted the potential regulatory schemes in fungal pathogenesis. Each fish was intraperitoneally injected with C. albicans cells and these infected fish were collected at 0.5, 1, 2, 4, 6, 8, 12, 16, 18 hpi. 0.625M-NM-<g of Cy3 cRNA for C. albicans array and 1.65 M-NM-<g of Cy3 cRNA for zebrafish array was fragmented to an average size of about 50-100 nucleotides by incubation with fragmentation buffer at 60M-BM-0C for 30 minutes. Each time points contain three biological repeat. For C. albicans array, each biological repeat has two technical replicates.
2013-08-26 | E-GEOD-32117 | biostudies-arrayexpress