Neutrophil activation by IL-4, IL-13 and IFN-g
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA904260 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22375779.fastq.gz | Fastqsanger.gz | |||
| SRR22375779_1.fastq.gz | Fastqsanger.gz | |||
| SRR22375779_2.fastq.gz | Fastqsanger.gz | |||
| SRR22375780_1.fastq.gz | Fastqsanger.gz | |||
| SRR22375780_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 37 |
Similar Datasets
Project description:Interleukin (IL)-4 and IL-13 are related cytokines with well-known roles in type 2 immune response. However, their effects on neutrophils are less defined and existing research has provided somewhat contradictory results We measured IL-4-, IL-13- and IFN-g-stimulated gene expression in highly purified human neutrophils.
2023-03-28 | GSE218535 | GEO
Project description:We used ChIP-seq to investigate epigenomic modifications in response to IFN-a, IL-17, and IL-13 in primary human bronchial epithelial cells (HBECs).
2022-05-24 | GSE185201 | GEO
Project description:We used bulk cell RNA-seq to investigate transcriptional effects of IFN-a, IL-17, and IL-13 in primary human bronchial epithelial cells (HBECs).
2022-05-24 | GSE185200 | GEO
Project description:We used scRNA-seq to investigate cell type-specific transcriptional effects of IFN-a, IL-17, and IL-13 in primary human bronchial epithelial cells (HBECs).
2022-05-24 | GSE185199 | GEO
Project description:The clinical features of psoriasis, characterized by sharply demarcated scaly erythematous plaques, are typically so distinctive that a diagnosis can easily be made on these grounds alone. However, there is great variability in treatment response between individual patients, and this may reflect heterogeneity of inflammatory networks driving the disease. In this study, whole-genome transcriptional profiling was used to characterize inflammatory and cytokine networks in 62 lesional skin samples obtained from patients with stable chronic plaque psoriasis. We were able to stratify lesions according to their inflammatory gene expression signatures, identifying those associated with strong (37% of patients), moderate (39%) and weak inflammatory infiltrates (24%). Additionally, we identified differences in cytokine signatures with heightened cytokine-response patterns in one sub-group of lesions (IL-13-strong; 50%) and attenuation of these patterns in a second sub-group (IL-13-weak; 50%). These sub-groups correlated with the composition of the inflammatory infiltrate, but were only weakly associated with increased risk allele frequency at some psoriasis susceptibility loci (e.g., REL, TRAF3IP2 and NOS2). Our findings highlight variable points in the inflammatory and cytokine networks known to drive chronic plaque psoriasis. Such heterogeneous aspects may shape clinical course and treatment responses, and can provide avenues for development of personalized treatments. We used Affymetrix microarrays to evaluate genome-wide expression in primary human keratinocytes exposed to cytokines. Cytokine activity signatures were used to interpret the shifts in gene expression that occur in psoriasis plaques relative to normal uninvolved skin. Primary keratinocytes from three donors (subjects 1, 2, and 3) were obtained and were either untreated (control) or exposed to cytokines (IL-4, IL-13, IFN-alpha, IFN-gamma and TNF). For the IL17A samples, primary keratinocytes were obtained from six donors, with cells derived from three donors treated with IL-17A and cells derived from the other three donors left untreated (i.e., unpaired control samples).
2012-03-07 | E-GEOD-36287 | biostudies-arrayexpress
Project description:High salt reduces the activation of IL-4+IL-13 stimulated macrophages
| PRJEB8115 | ENA
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:The cytokine environment and cellular infiltrate during an inflammatory response may contain prognostic features that could guide therapy or predict disease outcome. Here we analyzed the transcriptional responses of human monocytes, macrophages, dendritic cells and neutrophils to stimulation by type 1 cytokines (IFN-g, IFN-b and IFN-l) type 2 cytokines (IL-4 and IL-13) and the immunoregulatory cytokine IL-10. This generated a myeloid cell cytokine specific response matrix to infer representation of myeloid cells and the cytokine environment they may encounter during infection and in tumors. Neutrophils were surprisingly responsive to type 1 and type 2 cytokine stimulation but did not respond to IL-10. We identified transcripts specific to IFN-b stimulation, whereas other IFN signature genes were upregulated by both IFN-g and IFN-b. When used to deconvolute blood profiles from tuberculosis patients, the IFN-b specific neutrophil signature was surprisingly reduced in TB patients with active disease whereas the shared response to IFN-g and IFN-b in neutrophils was increased. When applied to glioma patients, transcripts of neutrophils exposed to IL-4 or IL-13 and monocyte responses to IFN-g or IFN-b emerged as opposing predictors of survival in samples from patients with glioma. This approach may help delineate biological roles for myeloid cells in different cytokine environments during disease processes.
2020-02-21 | GSE145647 | GEO
Project description:The cytokine environment and cellular infiltrate during an inflammatory response may contain prognostic features that could guide therapy or predict disease outcome. Here we analyzed the transcriptional responses of human monocytes, macrophages, dendritic cells and neutrophils to stimulation by type 1 cytokines (IFN-g, IFN-b and IFN-l) type 2 cytokines (IL-4 and IL-13) and the immunoregulatory cytokine IL-10. This generated a myeloid cell cytokine specific response matrix to infer representation of myeloid cells and the cytokine environment they may encounter during infection and in tumors. Neutrophils were surprisingly responsive to type 1 and type 2 cytokine stimulation but did not respond to IL-10. We identified transcripts specific to IFN-b stimulation, whereas other IFN signature genes were upregulated by both IFN-g and IFN-b. When used to deconvolute blood profiles from tuberculosis patients, the IFN-b specific neutrophil signature was surprisingly reduced in TB patients with active disease whereas the shared response to IFN-g and IFN-b in neutrophils was increased. When applied to glioma patients, transcripts of neutrophils exposed to IL-4 or IL-13 and monocyte responses to IFN-g or IFN-b emerged as opposing predictors of survival in samples from patients with glioma. This approach may help delineate biological roles for myeloid cells in different cytokine environments during disease processes.
2019-10-01 | GSE131990 | GEO
Project description:Skin barrier dysfunction initiates or deteriorates various cutaneous problems, such as atopic dermatitis (AD). In high concentrations, the nonreducing disaccharide α-d-glucopyranosyl α-d-glucopyranoside (trehalose) can induce transient senescence-like state in fibroblasts and promote wound repair. Here we have investigated the direct effect of a high concentration of trehalose on primary human keratinocytes (KCs) and demonstrated its specific role in the skin barrier. RNA-seq analysis revealed that trehalose regulates many skin-barrier-associated genes in T helper 2 (Th2) cytokines interleukin (IL)-4/IL-13-treated and -untreated KCs. Using monolayer-cultured post-confluent normal human KCs and living skin equivalent (LSE), we identified IL-4/IL-13-downregulated differentiation markers and various epidermal antimicrobial proteins, all of which were significantly upregulated or restored by trehalose (60 mg/mL). Trehalose inhibited IL-33 expression and reduced nuclear IL-33 by activating MEK5- extracellular signal-regulated kinase (ERK)-5 and suppressing MEK1/2-ERK pathways. It also increased nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase 1 (HMOX1) activation via c-Jun N-terminal kinase (JNK), thus, neutralizing IL-4/IL-13-mediated oxidative stress. Trehalose prevented IL-4/IL-13-mediated signal transducer and activator of transcription (STAT)3 and STAT6 activation and restored various skin barrier molecules reduced by IL-4/IL-13 via IL-33 downregulation and Nrf2-HMOX1 activation. This study demonstrates that trehalose might play salubrious roles as skin barrier repair in AD.
2024-09-30 | GSE244738 | GEO