Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA90051 | ENA |
REPOSITORIES: ENA
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Project description:The bacterial type III secretion system (TTSS) is dedicated to directly effect host cell pathways by pathogens. In order to identify the key host responses of the various parts of the TTSS, we utilized expression profiling of a lung pneumocytes cell line, A549, exposed to various isogenic mutant strains of Pseudomonas aeruginosa PAK. We have devised a novel filtering method to isolate the key responses to the effector proteins as well as the translocation machinery. Individually, the effector proteins elicited host responses that were consistent with the known function of each, many of which either regulated, or are regulated by the cell cycle. However, our analysis has shown that the effector proteins elicit a distinct host expression pattern when present in combination, suggesting that these proteins function in synergy. Furthermore, the host transcriptional response to the translocation complex involved genes that are involved in remodeling of the plasma membrane, suggesting that the host cell is able to sense the protrusion of the TTSS machinery. This study shows that the individual components of the TTSS define an integrated system and that a systems biology approach is required to fully understand the complex interplay between pathogen and host. Keywords = Pseudomonas aeruginosa Keywords = A549 human lung carcinoma cell line Keywords = cystic fibrosis Keywords: repeat sample
2004-12-10 | GSE1469 | GEO
Project description:The bacterial type III secretion system (TTSS) is dedicated to directly effect host cell pathways by pathogens. In order to identify the key host responses of the various parts of the TTSS, we utilized expression profiling of a lung pneumocytes cell line, A549, exposed to various isogenic mutant strains of Pseudomonas aeruginosa PAK. We have devised a novel filtering method to isolate the key responses to the effector proteins as well as the translocation machinery. Individually, the effector proteins elicited host responses that were consistent with the known function of each, many of which either regulated, or are regulated by the cell cycle. However, our analysis has shown that the effector proteins elicit a distinct host expression pattern when present in combination, suggesting that these proteins function in synergy. Furthermore, the host transcriptional response to the translocation complex involved genes that are involved in remodeling of the plasma membrane, suggesting that the host cell is able to sense the protrusion of the TTSS machinery. This study shows that the individual components of the TTSS define an integrated system and that a systems biology approach is required to fully understand the complex interplay between pathogen and host.
2007-08-03 | E-GEOD-1469 | biostudies-arrayexpress
Project description:Polymyxins are the last-line antibiotics against multidrug-resistant Pseudomonas aeruginosa however, resistance to polymyxins has been increasingly reported. Therefore, understanding the mechanisms of polymyxin activity and resistance is crucial for preserving their clinical usefulness. This study employed comparative metabolomics and transcriptomics to investigate the responses of polymyxin-susceptible PAK (polymyxin B MIC 1 mg/l) and its polymyxin-resistant pmrB mutant PAKpmrB6 (MIC 16 mg/l) to polymyxin B (4, 8, and 128 mg/l) at 1, 4, and 24h. Our results revealed that polymyxin B at 4 mg/l induced different metabolic and transcriptomic responses between polymyxin-susceptible and -resistant P. aeruginosa. In PAK, polymyxin B significantly activated PmrAB and the mediated arn operon, leading to increased 4-amino-4-deoxy-L-arabinose (L-Ara4N) synthesis and the addition to lipid A. On the contrary, polymyxin B did not increase lipid A modification in PAKpmrB6. Moreover, the syntheses of lipopolysaccharide and peptidoglycan were significantly decreased in PAK, but increased in PAKpmrB6 due to polymyxin B treatment. In addition, 4 mg/l polymyxin B significantly perturbed phospholipid and fatty acid levels and induced oxidative stress in PAK, but not in PAKpmrB6. Notably, the increased trehalose-6-phosphate levels indicate that polymyxin B potentially caused osmotic imbalance in both strains. Furthermore, 8 and 128 mg/l polymyxin B significantly elevated lipoamino acid levels and decreased phospholipid levels, but without dramatic changes in lipid A modification in both wildtype and mutant strains. Overall, this systems study is the first to elucidate the complex and dynamic interactions of multiple cellular pathways associated with polymyxin mode of action against P. aeruginosa.
2018-11-14 | MTBLS751 | MetaboLights
Project description:We have isolated and characterized several bacteriophages infecting Pseudomonas aeruginosa distantly related to Felix O1 virus and proposed they form a new subfamily named Felixounavirinae. The infectious cycle of bacteriophages belonging to this subfamily has not been studied yet in terms of gene expression. The present study reports the RNA-Seq analysis of bacteriophage PAK_P3 infecting PAK strain of P. aeruginosa. RNA profile of Host and Phage at 0min, 3.5min and 13 min after infection of Pseudomonas aeruginosa PAK strain with the Pseudomonas phage PAK P3. Three biological replicates for each time point.
2016-07-20 | E-GEOD-76513 | biostudies-arrayexpress
Project description:Primary pneumocytes from KRas;Atg5fl/+ and KRas;Atg5fl/fl littermates were cultured for 48 hours and infected with AdCre-GFP to induce expression of the KrasG12D oncogene and concomitant Atg5 deletion. The transcriptional profile of those cells was determined by mRNA sequencing and uncovered differential expression in cellular movement, inflammatory response and oxidative stress response. Comparison of transcriptomes from KRas;Atg5fl/+ and KRas;Atg5fl/fl pneumocytes
2014-01-07 | E-GEOD-48387 | biostudies-arrayexpress
Project description:Pseudomonas aeruginosa strain PAK and isogenic in-frame deletion mutants
| PRJNA978077 | ENA
Project description:NEDD9 is important for lung cancer metastasis. However, the detailed mechanism remains elusive. Using the microarray data generated with human lung cancer cell lines with either NEDD9 overexpression or NEDD9 knockdown, we plan to idnetify important signal pathways regulated by NEDD9. This may explain how NEDD9 excutes its function in lung cancer. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Human lung cancer cell line A549, which has LKB1 loss-of-function mutation and increased expression of NEDD9, was used for two individual NEDD9 knockdown. Human lung cancer cell line CRL-5907, which has wild-type LKB1 and low NEDD9 expression level, was used for NEDD9 overexpression. The microarray was done in A549 cells, A549 cells with two different NEDD9 knockdown; CRL-5907 cells and CRL-5907 cells with NEDD9 overexpression.
2013-02-21 | E-GEOD-26846 | biostudies-arrayexpress
Project description:RNA-seq of Human lung cell line A549 infected with Adenovirus
| PRJNA296866 | ENA
Project description:We have isolated and characterized several bacteriophages infecting Pseudomonas aeruginosa distantly related to Felix O1 virus and proposed they form a new subfamily named Felixounavirinae. The infectious cycle of bacteriophages belonging to this subfamily has not been studied yet in terms of gene expression. The present study reports the RNA-Seq analysis of bacteriophage PAK_P3 infecting PAK strain of P. aeruginosa.
2016-07-20 | GSE76513 | GEO
Project description:We have isolated and characterized several bacteriophages infecting Pseudomonas aeruginosa distantly related to Felix O1 virus and proposed they form a new subfamily named Felixounavirinae. The infectious cycle of bacteriophages belonging to this subfamily has not been studied yet in terms of gene expression. The present study reports the RNA-Seq analysis of bacteriophage PAK_P4 infecting PAK strain of P. aeruginosa.
2017-07-07 | GSE86022 | GEO