Transcription profiling of normal human monocytes in response to Aspergillus fumigatus
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Morten Mattingsdal
PROVIDER: E-MEXP-1103 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Aspergillus fumigatus is the most important pulmonary fungal pathogen. Virulence has evolved several times in the section Aspergillii. However, there are species in this section, such as A. fischerii and A. oerlinghausensis, that are very closely related to A. fumigatus but are not reported as pathogens. By using trypsin shaving, we have identified the proteins on the conidial surface of conidia and swollen conidia of A. fumigatus, A. fischeri, A. oerlinghausensis, and A. lentulus. We have identified about 900 proteins in all four species and shown 52 that are unique in A. fumigatus. Both A. fischerii and A. oerlinghausensis have homologues for most of these proteins. However, they are not expressed in the conidia and and could reflect specific A. fumigatus traits important for infection and/or immune evasion.
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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.).
2005-05-15 | E-MEXP-332 | biostudies-arrayexpress
Project description:Immune inertness of Aspergillus fumigatus conidia, an airborne fungal pathogen, is attributed to its surface rodlet-layer made up of RodAp, a protein belonging to the hydrophobin family, characterized by eight conserved cysteine residues forming four disulfide bonding. Earlier, we showed that the conserved cysteine residue point (ccrp) mutations result in conidia devoid of the rodlet-layer. Here we extended our study in comparing ccrp-mutation with RODA deletion on their mutant conidial surface organization, permeability and immunoreactivity. Western blot using anti-RodAp antibodies indicated the absence of RodAp in the cytoplasm of ccrp-mutant conidia. Upon immunolabelling, ccrp-mutant conidia showed strong positivity for -(1,3)-glucan and weak positivity for -(1,3)-glucan, which was reverse in ∆rodA conidia, and the parental strain conidia were negative; all of their conidial cell wall permeability was similar. Proteomic analyses of the conidial surface exposed proteins of the ccrp-mutants, although lower in number, showed more similarities with the parental strain, but a significant difference with the RODA deletion mutant strain. Further, ccrp-mutant conidia are less immunostimulatory compared to ∆rodA conidia. Together, our data suggest that (i) the conserved cysteine residues are essential for the trafficking of RodAp and the organization of rodlet-layer on the conidial surface, and (ii) point-mutation could be an alternative strategy to study the proteins involved in the organization of fungal cell wall.
2021-02-18 | PXD020136 | Pride
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).
2010-10-29 | E-GEOD-24984 | biostudies-arrayexpress
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:Aspergillus fumigatus is a filamentous fungus capable to cause an important disease known as invasive aspergillosis. Challenge different cell lines is a crucial strategy to undercover new virulence factors involved in the infection process. In this research, RAW 264.7 macrophages and A549 lung epithelial cells were challenge using A. fumigatus conidia in a MOI of 10 and 5 respectively. When these conidia reach 30% of germination, the total RNA was isolated (A. fumigatus alone (Control), A. fumigatus vs RAW 264.7, and A. fumigatus vs A549) and purified using the RNeasy Plant Mini Kit (Qiagen). The AWAFUGE (Agilent Whole A. fumigatus Genome Expression 44K v.1) hybridization was carried out following previously publish protocols (A-MEXP-2352 and E-MTAB-5314).
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Project description:Investigation of whole genome gene expression level changes in trichostatin A (TSA)-treated A. fumigatus Af293 compared to non-treated A. fumigatus Af293. Species: Aspergillus fumigatus; Strain: Af293; Type of array: Eukaryotic Expression (4plex, 2plex for a TSA-treated sample and 2plex for a non-treated sample); Technical replicates: Two per treatment.
2010-06-30 | E-GEOD-19682 | 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:An Aspergillus fumigatus infection is initialized by the inhalation and germination of airborne asexual spores (conidia). Alveolar macrophages are the first immune cells to counteract an infection by phagocytosis of conidia and intracellular degradation of the pathogen. However, A. fumigatus circumvents its intracellular killing by the manipulation of the phagolysosomal maturation. With a comparative proteomic study of the phagolysosomal proteome of a virulent wild type A. fumigatus strain and an avirulent mutant strain we aimed at the identification of proteins and processes that are hijacked by the virulent strain. We found that wild type conidia strongly modulate the protein composition of the phagolysosome. Assembly and activity of vATPase, formation of lipid rafts, signal transduction pathways as well as the generation of energy and metabolites were significantly regulated in the wild type conidia containing phagolysosomes. In different experimental setups we confirmed a disassembly of the vATPase complex, reduced formation of lipid rafts and altered abundances of mTOR, MAPK signaling molecules, Rab5 and Vamp8 mediators of endosomal trafficking as well as LAMP1 and cathepsin Z lysosomal markers. Our interactome analysis indicates that A. fumigatus proteins target small GTPases of the endosomal trafficking system and signal transducers of the host, which might lead to a reduced fungicidal activity of the phagolysosome.
2018-03-08 | PXD005724 | Pride
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).
2010-10-29 | E-GEOD-24985 | biostudies-arrayexpress