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Project description:Gene expression by Aspergillus protease
| PRJNA774169 | ENA
Project description:<h4><strong>BACKGROUND: </strong>Several studies have shown a correlation between an altered metabolome and respiratory allergies. The epithelial barrier hypothesis proposes that an epithelial barrier dysfunction can result in allergic diseases development. Der p 1 allergen from house dust mite is a renowned epithelial barrier disruptor and allergy initiator due to its cysteine-protease activity. Here, we compared the metabolic profile of the bronchial epithelium exposed or not to Der p 1 during barrier establishment to understand its active role in allergy development.</h4><h4><strong>METHODS: </strong>Calu-3 cells were cultivated in air-liquid interface cultures and exposed to either Der p 1 or Ole e 1 allergens during barrier establishment. The comparative metabolomics analysis of apical and basolateral media were performed using liquid chromatography and capillary electrophoresis both coupled to mass spectrometry.</h4><h4><strong>RESULTS: </strong>We showed that epithelial barrier disruption by Der p 1 was associated with a specific metabolic profile, which was highly dependent on the state of the epithelium at the time of contact. Moreover, an apical-basolateral distribution of the metabolites was also observed, indicating a compartmentalization of the response with differential metabolic patterns. A number of metabolites were changed by Der p 1, mainly related to amino acids metabolism, such as L-arginine, L-kynurenine and L-methionine.</h4><h4><strong>CONCLUSION: </strong>This work is the first report on the metabolic response in human bronchial epithelial cells associated with cysteine-protease Der p 1 activity, which could contribute to allergy development. Moreover, it supports a reformulated epithelial barrier hypothesis that might help to explain allergies and their increasing prevalence.</h4>
2023-08-22 | MTBLS1755 | MetaboLights
Project description:Aspergillus fumigatus is the most common opportunistic mold pathogen of humans, causing invasive diseases in immunocompromised patients. In these patients, the fungus can invade the lungs and other organs, causing severe damage. Penetration of the pulmonary epithelium is a key step in the infectious process. A. fumigatus produces extracellular proteases to degrade the structural barriers of the host. The A. fumigatus transcription factor PrtT controls the expression of multiple secreted proteases. PrtT shows similarity to the fungal Gal4-type Zn(2)-Cys(6) DNA-binding domain of several transcription factors. In this work, we further investigate the function of this transcription factor by performing a transcriptional and a proteomic analysis of the ΔprtT mutant. The microarray analysis revealed several unexpected findings. In addition to a decrease in protease expression, expression of genes involved in iron uptake and ergosterol synthesis was dramatically decreased in the ΔprtT mutant. A second finding of interest is that deletion of PrtT resulted in the upregulation of four secondary metabolite clusters, including genes for the biosynthesis of pseurotin A. The proteomic analysis identified 15 proteins secreted by the A. fumigatus WT strain when grown on protein-rich skim-milk medium. Of these, the ΔprtT mutant expressed reduced levels of ALP1 protease, TppA tripeptidyl peptidase and a serine peptidase and increased levels of FAD-oxygenase, AspF chitosinase, EglC endoglucanase and Bgt1 glucanosyltransferase compared to the WT strain. This report highlights the complexity of gene regulation by PrtT.
2011-11-29 | GSE33254 | GEO
Project description:In the present study, we hypothesized that C/EBPa (CCAAT/enhancer-binding protein alpha) plays a role in cell regeneration in response to bronchiolar epithelial cell injury. C/EBPa mediated ciliated cell regeneration after naphthalene bronchiolar epithelial cell injury in vivo. Furthermore, we demonstrated that C/EBPa regulates protease/anti-protease balance after lung injury, and intratracheal treatment with anti-protease (BPTI) restored ciliated cell regeneration after naphthalene injury in CebpaD/D mice.
2012-05-13 | GSE29285 | GEO
Project description:In the present study, we hypothesized that C/EBPa (CCAAT/enhancer-binding protein alpha) plays a role in cell regeneration in response to bronchiolar epithelial cell injury. C/EBPa mediated ciliated cell regeneration after naphthalene bronchiolar epithelial cell injury in vivo. Furthermore, we demonstrated that C/EBPa regulates protease/anti-protease balance after lung injury, and intratracheal treatment with anti-protease (BPTI) restored ciliated cell regeneration after naphthalene injury in CebpaD/D mice. Cebpa d/d VS. Control mice 0hr, 3hr and 72hr after naphthalene injury. Three replicates each.
2012-05-12 | E-GEOD-29285 | biostudies-arrayexpress
Project description:Functional genomics of Aspergillus fumigatus conidiospores interacting with human bronchial epithelial cells
| PRJNA122795 | ENA
Project description:Investigation of whole genome gene expression level changes in Aspergillus nidulans OE::rsmA compared to wild-type RDIT9.32 (veA). A twelve array study using total RNA recovered from six separate cultures of Aspergillus nidulans wild-type RDIT9.32 (veA) and six separate cultures of Aspergillus nidulans overexpressing rsmA (restorer of secondary metabolism A), using custom-designed, four-plex arrays. The experiment was divided into two runs. In the first run, three biological replicates each of Aspergillus nidulans wild-type RDIT9.32 (veA) and Aspergillus nidulans carrying a plasmid overexpressing rsmA under the control of the gpdA promoter were assayed. In the second run, three biological replicates each of Aspergillus nidulans wild-type RDIT9.32 (veA) and Aspergillus nidulans overexpressing rsmA at the native locus under the control of the gpdA promoter were assayed.
2012-01-17 | E-GEOD-34220 | biostudies-arrayexpress
Project description:Determine if transcripts are released by protease treatment Keywords: Comparison of protease treatments
2005-12-01 | GSE3686 | GEO
Project description:The goal of this study is to determine the transcriptional response of primary normal human bronchial epithelial (NHBE) cells following interaction with A. fumigatus conidia at 2, 6, and 12 hours in order to examine the infection of airway epithelial cells at multiple time points of co-incubation. After total RNA isolation, the Illumina® HiSeq 2000 next generation sequencing system was used to characterize the transcriptional response, in untreated and A. fumigatus exposed cells.
2017-09-21 | GSE61955 | GEO
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 ΔPrtT 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.
2010-10-29 | GSE24985 | GEO