Transcriptomic analysis of A. fumigatus without or with ETD151 (0.156 µM) or amphotercin B (1.1µM)
Ontology highlight
ABSTRACT:
INSTRUMENT(S): DESeq2, NextSeq 500
ORGANISM(S): Aspergillus fumigatus
SUBMITTER: Juliette Guitard
PROVIDER: E-MTAB-15319 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Response of A549 cells treated with Aspergillus fumigatus germinating conidia (WT-GC) or culture filtrate (WT-CF) for 8h Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ÎPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF treatment in a protease-dependent manner. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications. 3 independent controls (uninfected A549 cells) as ctrl2_1-3, 2 independent treatments of A549 cells with wild-type A. fumigatus culture filtrates (WT-CF2_1-2) and 2 independent treatments of A549 cells with wild-type A. fumigatus germinating conidia (WT-GC_2-3).
2010-10-29 | E-GEOD-24983 | biostudies-arrayexpress
Project description:Response of A549 cells treated with Aspergillus fumigatus wild type culture filtrate (WT-CF) or PrtT protease deficient mutant culture filtrate (PrtT-CF) for 8h Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ÎPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF treatment in a protease-dependent manner. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications. 3 independent controls (uninfected A549 cells) as ctrl2_1-3, 3 independent treatments of A549 cells with wild-type A. fumigatus culture filtrates (WT-CF1_1-3) and 2 independent treatments of A549 cells with A. fumigatus prtT mutant culture filtrates (PrtT-CF_1-2).
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Project description:Response of A549 cells treated with Aspergillus fumigatus wild type germinating conidia (WT_GC) or PrtT protease deficient mutant conidia (PrtT-GC) or inert acrylic 2-4 micron beads (Beads) for 8h Aspergillus fumigatus is the most commonly encountered mold pathogen of humans, predominantly infecting the respiratory system. Colonization and penetration of the lung alveolar epithelium is a key but poorly understood step in the infection process. This study focused on identifying the transcriptional and cell-signaling responses activated in A549 alveolar carcinoma cells incubated in the presence of A. fumigatus wild-type and ÎPrtT protease-deficient germinating conidia and culture filtrates (CF). Microarray analysis of exposed A549 cells identified distinct classes of genes whose expression is altered in the presence of germinating conidia and CF and suggested the involvement of both NFkB and MAPK signaling pathways in mediating the cellular response. Phosphoprotein analysis of A549 cells confirmed that JNK and ERK1/2 are phosphorylated in response to CF treatment in a protease-dependent manner. Inhibition of JNK or ERK1/2 kinase activity substantially decreased CF-induced cell damage, including cell peeling, actin-cytoskeleton damage, and reduction in metabolic activity and necrotic death. These results suggest that inhibition of MAPK-mediated host responses to treatment with A. fumigatus CF decreases cellular damage, a finding with possible clinical implications. 2 independent controls (uninfected A549 cells) as ctrl3_1-2, 2 independent treatments of A549 cells with wild-type A. fumigatus germinating conidia (WT_GC_1-2 ) , 2 independent treatments of A549 cells with inert acrylic beads (Beads 1-2), 3 independent treatments of A549 cells with A. fumigatus prtT mutant germinating conidia (PrtT-GC_1-3).
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Project description:This SuperSeries is composed of the following subset Series: GSE24983: Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_WT-GC] GSE24984: Response of A549 cells treated with Aspergillus fumigatus [WT-GC_vs_PrtT-GC] GSE24985: Response of A549 cells treated with Aspergillus fumigatus [WT-CF_vs_PrtT-CF] Refer to individual Series
2010-10-29 | E-GEOD-24986 | biostudies-arrayexpress
Project description:Genomic DNA from five strains, Aspergillus fumigatus Af71, Aspergillus fumigatus Af294, Aspergillus clavatus, Neosartorya fenneliae, and Neosartorya fischeri, were co-hybridized with that of Aspergillus fumigatus Af293 and compared.
2005-05-15 | E-MEXP-333 | biostudies-arrayexpress
Project description:Experimental factor: Time after the temperature shift from 30C to 37C or 30C to 48C. Conidia (5x106 /ml) from Aspergillus fumigatus Af293 were incubated in the CM medium for germination (~ 17 hrs) at 30C. The culture was transferred to a water bath of 37C or 48C for continued growth. Samples were taken after the defined time (i.e. 0, 15, 30, 60, 120, and 180 min.).
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Project description:Aspergillus fumigatus contributes to invasive and allergic pulmonary disease in immunocompromised individuals. The pulmonary mucus of cystic fibrosis (CF) patients displays elevated levels of the pleiotropic cathelicidin antimicrobial peptide LL-37 and the aim of this work was to assess the effect of LL-37 on the growth A. fumigatus. Exposure of A. fumigatus conidia to high concentrations of intact LL-37 (100 μg/ml) for 24 hours had a positive effect on growth (277.45 ± 22.59% (p < 0.01)) whereas scrambled LL-37 (76.45 ± 7.46%) did not. Exposure of 24 hour pre-formed mycelium to 5 μg/ml LL-37 for 48 hours increased hyphal wet weight significantly (4.37 ± 0.23 g, p < 0.001) compared to the control (2.67 ± 0.05 g). Amino acid leakage from mycelium was observed in the presence of LL-37 and gliotoxin secretion was increased at 24 hours from LL-37 exposed hyphae (169.1 ± 6.36 ng/mg hyphae, p < 0.05) compared to the control (102 ± 18.81 ng/mg hyphae). Quantitative proteomic analysis of 24 hour LL-37 treated hyphae revealed an increase in the abundance of proteins associated with growth (eIF-5A (16.3 fold increased), tissue degradation (aspartic endopeptidase (4.7 fold increased)) and allergic reactions (Asp F13 (10 fold increased)). By 48 hours there was an increase in proteins indicative of cellular stress (glutathione peroxidase (9 fold increased)), growth (eIF-5A (6 fold increased), and virulence (ribonuclease mitogillin (3.7 fold increased). These results indicate that LL-37 stimulates A. fumigatus growth and this may result in increased fungal growth and secretion of toxins in the lungs of CF patients.
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