Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA121229 | ENA |
REPOSITORIES: ENA
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Project description:The establishment of bacterial infections at epithelial surfaces is determined by the balance of virulence attributes of the pathogen with the activity of innate host defenses. Polymorphonuclear leukocytes (PMN) are key responders in many bacterial infections, but the mechanisms by which pathogens subvert these early responses to establish infection are largely undefined. Here, we model these early interactions between human PMN and the primary cause of urinary tract infections, namely uropathogenic Escherichia coli (UPEC). Our objective was to define virulence phenotypes of uropathogens (as compared with laboratory and commensal E. coli strains) that permit evasion of PMN activity. We found that UPEC strains resist phagocytic killing and dampen the production of antimicrobial reactive oxygen species by PMNs. Analysis of the global transcriptional responses of PMN to E. coli strains revealed that UPEC exposure downregulates the expression of PMN genes involved in proinflammatory signaling and PMN chemotaxis, adhesion, and migration. Consistent with these data, UPEC attenuated transepithelial neutrophil recruitment in an in vitro model of acute infection. We propose that these UPEC strategies are important in the establishment of epithelial infection, and that the findings are germane to a range of bacterial infections at epithelial surfaces. We used microarrays to detail the global program of gene expression in human neutrophils in response to a uropathogenic bacteria compared to a closely related non-pathogenic strain relative to control samples with no bacteria. Our goal was to elucidate a pathogen-specific response. We chose an early time point of 60 minutes to evaluate the accute response to infection. Human neutrophils were exposed to pathogenic or commensal Escherichia coli for RNA extraction and hybridization on Affymetrix microarrays
2010-03-07 | E-GEOD-18810 | biostudies-arrayexpress
Project description:Intercalated cells are known to be involved in acid-base homeostasis via vacuolar ATPase (H+-ATPase or V-ATPase) expression. Increasing evidence supports an innate immune role for ICs along with their traditional function of pH regulation. In this study, human kidney tissue was enriched for viable intercalated cells then exposed to uropathogenic E. coli versus saline control. Single cell transcriptomics was performed. Six intercalated cell subtypes were identified including hybrid principal-intercalated cells. Cell specific cluster marker gene list generated from this sequencing data was put through ingenuity pathway analysis pipeline which predicted “phagosome maturation” as a key biological pathway that increased in rank following exposure to uropathogenic E. coli in two of the intercalated cell subtypes. Uptake of E. coli and pHrodo coated E. coli BioParticlesTM during live animal intravital microscopy demonstrated that intercalated cell phagocytosis of bacteria was an active process that involved acidification. Taken together, our finding indicate that intercalated cells represent an epithelial cell with characteristics of professional phagocytes like macrophages or neutrophils, which includes the ability to phagocytose E. coli and acidify phagolysosomes.
2020-10-22 | GSE159805 | GEO
Project description:Identification and expression analysis of microRNAs in infected larvae of the insect model Galleria mellonella with uropathogenic (UPEC) and commensal E. coli strains that are known to cause symptomatic and asymptomatic bacteriuria (ABU) in humans, respectively.
2018-12-18 | GSE123965 | GEO
Project description:Gene expression data from S. aureus-exposed neutrophils
| PRJNA117601 | ENA
Project description:Gene expression data from F. tularensis-exposed neutrophils
| PRJNA159947 | ENA
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:The establishment of bacterial infections at epithelial surfaces is determined by the balance of virulence attributes of the pathogen with the activity of innate host defenses. Polymorphonuclear leukocytes (PMN) are key responders in many bacterial infections, but the mechanisms by which pathogens subvert these early responses to establish infection are largely undefined. Here, we model these early interactions between human PMN and the primary cause of urinary tract infections, namely uropathogenic Escherichia coli (UPEC). Our objective was to define virulence phenotypes of uropathogens (as compared with laboratory and commensal E. coli strains) that permit evasion of PMN activity. We found that UPEC strains resist phagocytic killing and dampen the production of antimicrobial reactive oxygen species by PMNs. Analysis of the global transcriptional responses of PMN to E. coli strains revealed that UPEC exposure downregulates the expression of PMN genes involved in proinflammatory signaling and PMN chemotaxis, adhesion, and migration. Consistent with these data, UPEC attenuated transepithelial neutrophil recruitment in an in vitro model of acute infection. We propose that these UPEC strategies are important in the establishment of epithelial infection, and that the findings are germane to a range of bacterial infections at epithelial surfaces. We used microarrays to detail the global program of gene expression in human neutrophils in response to a uropathogenic bacteria compared to a closely related non-pathogenic strain relative to control samples with no bacteria. Our goal was to elucidate a pathogen-specific response. We chose an early time point of 60 minutes to evaluate the accute response to infection.
2010-03-01 | GSE18810 | GEO
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description:Kynureninase is a member of a large family of catalytically diverse but structurally homologous pyridoxal 5'-phosphate (PLP) dependent enzymes known as the aspartate aminotransferase superfamily or alpha-family. The Homo sapiens and other eukaryotic constitutive kynureninases preferentially catalyze the hydrolytic cleavage of 3-hydroxy-l-kynurenine to produce 3-hydroxyanthranilate and l-alanine, while l-kynurenine is the substrate of many prokaryotic inducible kynureninases. The human enzyme was cloned with an N-terminal hexahistidine tag, expressed, and purified from a bacterial expression system using Ni metal ion affinity chromatography. Kinetic characterization of the recombinant enzyme reveals classic Michaelis-Menten behavior, with a Km of 28.3 +/- 1.9 microM and a specific activity of 1.75 micromol min-1 mg-1 for 3-hydroxy-dl-kynurenine. Crystals of recombinant kynureninase that diffracted to 2.0 A were obtained, and the atomic structure of the PLP-bound holoenzyme was determined by molecular replacement using the Pseudomonas fluorescens kynureninase structure (PDB entry 1qz9) as the phasing model. A structural superposition with the P. fluorescens kynureninase revealed that these two structures resemble the "open" and "closed" conformations of aspartate aminotransferase. The comparison illustrates the dynamic nature of these proteins' small domains and reveals a role for Arg-434 similar to its role in other AAT alpha-family members. Docking of 3-hydroxy-l-kynurenine into the human kynureninase active site suggests that Asn-333 and His-102 are involved in substrate binding and molecular discrimination between inducible and constitutive kynureninase substrates.
| S-EPMC2531291 | biostudies-literature
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO