Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA128555 | ENA |
REPOSITORIES: ENA
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Project description:Despite the appreciated in vivo role of the redox-active Pseudomonas virulence factor pyocyanin in Pseudomonas airway infections and the recognized importance of airway epithelial cells in combating bacterial pathogens, little is known about pyocyaninM-bM-^@M-^Ys effect on airway epithelial cells. We find that exposure of bronchiolar epithelial cells to pyocyanin results in MUC2/MUC5AC induction and mucin secretion mediated by reactive oxygen species production, activation of the epidermal growth factor receptor pathway and release of inflammatory cytokines (IL-1b, IL-6, TGFa, TNFa). Microarray analysis identified 286 pyocyanin-induced genes in airway epithelial cells, including many of the inflammatory mediators elevated in cystic fibrosis airways (G-CSF, GM-CSF, CXCL1, SAA). We also found several novel pyocyanin-responsive genes of potential importance in the infection process (IL-24, CXCL2, CXCL3, CCL20, SOD2). This comprehensive study uncovers numerous details of pyocyaninM-bM-^@M-^Ys proinflammatory action and establishes airway epithelial cells as key responders following exposure to this microbial toxin. H292 cells were treated with or without 8 uM pyocyanin for 48 hrs in serum-free RPMI medium. RNA was isolated in four independent experiments, collected, processed and subjected to microarray analysis simultaneously (biological repeats).
2011-06-01 | E-GEOD-22430 | biostudies-arrayexpress
Project description:Despite the appreciated in vivo role of the redox-active Pseudomonas virulence factor pyocyanin in Pseudomonas airway infections and the recognized importance of airway epithelial cells in combating bacterial pathogens, little is known about pyocyanin’s effect on airway epithelial cells. We find that exposure of bronchiolar epithelial cells to pyocyanin results in MUC2/MUC5AC induction and mucin secretion mediated by reactive oxygen species production, activation of the epidermal growth factor receptor pathway and release of inflammatory cytokines (IL-1b, IL-6, TGFa, TNFa). Microarray analysis identified 286 pyocyanin-induced genes in airway epithelial cells, including many of the inflammatory mediators elevated in cystic fibrosis airways (G-CSF, GM-CSF, CXCL1, SAA). We also found several novel pyocyanin-responsive genes of potential importance in the infection process (IL-24, CXCL2, CXCL3, CCL20, SOD2). This comprehensive study uncovers numerous details of pyocyanin’s proinflammatory action and establishes airway epithelial cells as key responders following exposure to this microbial toxin.
2011-06-01 | GSE22430 | GEO
Project description:Transcription profiling of human airway epithelial cell-conditioned monocyte-derive dendritic cells
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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.
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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:Transcriptional profiling of Homo sapiens inflammatory skin diseases (whole skin biospies): Psoriasis (Pso), vs Atopic Dermatitis (AD) vs Lichen planus (Li), vs Contact Eczema (KE), vs Healthy control (KO) In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation. In recent years, different genes and proteins have been highlighted as potential biomarkers for psoriasis, one of the most common inflammatory skin diseases worldwide. However, most of these markers are not psoriasis-specific but also found in other inflammatory disorders. We performed an unsupervised cluster analysis of gene expression profiles in 150 psoriasis patients and other inflammatory skin diseases (atopic dermatitis, lichen planus, contact eczema, and healthy controls). We identified a cluster of IL-17/TNFα-associated genes specifically expressed in psoriasis, among which IL-36γ was the most outstanding marker. In subsequent immunohistological analyses IL-36γ was confirmed to be expressed in psoriasis lesions only. IL-36γ peripheral blood serum levels were found to be closely associated with disease activity, and they decreased after anti-TNFα-treatment. Furthermore, IL-36γ immunohistochemistry was found to be a helpful marker in the histological differential diagnosis between psoriasis and eczema in diagnostically challenging cases. These features highlight IL-36γ as a valuable biomarker in psoriasis patients, both for diagnostic purposes and measurement of disease activity during the clinical course. Furthermore, IL-36γ might also provide a future drug target, due to its potential amplifier role in TNFα- and IL-17 pathways in psoriatic skin inflammation.
2014-12-02 | GSE63741 | GEO
Project description:RNA sequencing of purified intestinal epithelial cells from paediatric biopsies including Inflammatory Bowel Disease and healthy controls
2025-01-23 | E-MTAB-5464 | ExpressionAtlas