Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA117615 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was “cell movement” including E-selectin, which was coordinately regulated with IL-1. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1, which together with IFN-, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease. 6 ENL skin lesions and 7 Lepromatous leprosy skin lesions
2009-06-30 | E-GEOD-16844 | biostudies-arrayexpress
Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was 'cell movement' including E-selectin, which was coordinately regulated with IL-1beta. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1beta, which together with IFN-gamma, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease.
2009-06-30 | GSE16844 | GEO
Project description:Tissue repair requires the resolution of inflammation. However, the molecular mechanisms that attenuate inflammation in vivo are not fully understood. Here, we identify that glutamine metabolism suppresses neutrophil recruitment to abrogate inflammation and drive tissue repair. Integrated metabolomic and transcriptional profiling identified glutamine metabolism as a key feature of macrophages during inflammatory resolution. Dietary depletion studies and conditional deletion of glutaminase (Gls), the essential enzyme involved in glutamine metabolism, in innate immune cells in mice reveals an essential role for glutamine metabolism in suppressing inflammation and promoting tissue repair. Genes involved in neutrophil recruitment are upregulated in macrophages lacking Gls and in foot ulcers of diabetic patients. Multimodal single cell transcriptomics and epigenomics reveals that Gls is required for chromatin remodeling of neutrophil recruitment genes in innate immune cells during resolution of inflammation. These findings highlight the role of glutamine metabolism in controlling cellular communication during tissue repair and suppressing neutrophil recruitment to advance inflammation resolution.
2026-02-01 | GSE289135 | GEO
Project description:Tissue repair requires the resolution of inflammation. However, the molecular mechanisms that attenuate inflammation in vivo are not fully understood. Here, we identify that glutamine metabolism suppresses neutrophil recruitment to abrogate inflammation and drive tissue repair. Integrated metabolomic and transcriptional profiling identified glutamine metabolism as a key feature of macrophages during inflammatory resolution. Dietary depletion studies and conditional deletion of glutaminase (Gls), the essential enzyme involved in glutamine metabolism, in innate immune cells in mice reveals an essential role for glutamine metabolism in suppressing inflammation and promoting tissue repair. Genes involved in neutrophil recruitment are upregulated in macrophages lacking Gls and in foot ulcers of diabetic patients. Multimodal single cell transcriptomics and epigenomics reveals that Gls is required for chromatin remodeling of neutrophil recruitment genes in innate immune cells during resolution of inflammation. These findings highlight the role of glutamine metabolism in controlling cellular communication during tissue repair and suppressing neutrophil recruitment to advance inflammation resolution.
2026-02-01 | GSE289255 | GEO
Project description:To study pathways associated with ferroptosis sensitivity
2022-06-01 | GSE173905 | GEO
Project description:Tissue repair requires the resolution of inflammation. However, the molecular mechanisms that attenuate inflammation in vivo are not fully understood. Here, we identify that glutamine metabolism suppresses neutrophil recruitment to abrogate inflammation and drive tissue repair. Integrated metabolomic and transcriptional profiling identified glutamine metabolism as a key feature of macrophages during inflammatory resolution. Dietary depletion studies and conditional deletion of glutaminase (Gls), the essential enzyme involved in glutamine metabolism, in innate immune cells in mice reveals an essential role for glutamine metabolism in suppressing inflammation and promoting tissue repair. Genes involved in neutrophil recruitment are upregulated in macrophages lacking Gls and in foot ulcers of diabetic patients. Multimodal single cell transcriptomics and epigenomics reveals that Gls is required for chromatin remodeling of neutrophil recruitment genes in innate immune cells during resolution of inflammation. These findings highlight the role of glutamine metabolism in controlling cellular communication during tissue repair and suppressing neutrophil recruitment to advance inflammation resolution.
2026-02-01 | GSE289254 | GEO
Project description:Tissue repair requires the resolution of inflammation. However, the molecular mechanisms that attenuate inflammation in vivo are not fully understood. Here, we identify that glutamine metabolism suppresses neutrophil recruitment to abrogate inflammation and drive tissue repair. Integrated metabolomic and transcriptional profiling identified glutamine metabolism as a key feature of macrophages during inflammatory resolution. Dietary depletion studies and conditional deletion of glutaminase (Gls), the essential enzyme involved in glutamine metabolism, in innate immune cells in mice reveals an essential role for glutamine metabolism in suppressing inflammation and promoting tissue repair. Genes involved in neutrophil recruitment are upregulated in macrophages lacking Gls and in foot ulcers of diabetic patients. Multimodal single cell transcriptomics and epigenomics reveals that Gls is required for chromatin remodeling of neutrophil recruitment genes in innate immune cells during resolution of inflammation. These findings highlight the role of glutamine metabolism in controlling cellular communication during tissue repair and suppressing neutrophil recruitment to advance inflammation resolution.
2026-02-01 | GSE289200 | 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: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