Ontology highlight
ABSTRACT:
PROVIDER: PRJNA655808 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12406764.fastq.gz | Fastqsanger.gz | |||
| SRR12406765.fastq.gz | Fastqsanger.gz |
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Project description:Reveal differentially regulated genes and cellular pathways within allergic and non-allergic asthmatic children compared to healthy controls Peripheral blood mononuclear cells (PBMCs) were obtained from allergic asthmatics (n=14), non-allergic asthmatics (n=8) and healthy controls (n=14) and kept with anti-CD3/CD28 (CD328), LpA or without stimulation (M).
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Project description:VAF347 is a low molecular weight compound which inhibits allergic lung inflammation in vivo. This effect is likely due to a block of dendritic cell (DC) function to generate pro-inflammatory T-helper (Th) cells since VAF347 inhibits IL-6, CD86 and HLA-DR expression by human monocyte derived DC, three relevant molecules for Th-cell generation. Here we demonstrate that VAF347 interacts with the aryl hydrocarbon receptor (AhR) protein resulting in activation of the AhR signaling pathway. Functional AhR is responsible for the biological activity of VAF347 since, i) other AhR agonists display an identical activity profile in vitro, ii) gene silencing of wild type AhR expression or forced over-expression of a trans-dominant negative AhR ablates VAF347 activity to inhibit cytokine induced IL-6 expression in a human monocytic cell line and iii) AhR deficient mice are resistant to the compoundâs ability to block allergic lung inflammation in vivo. These data identify the AhR protein as key molecular target of VAF347 and its essential role for mediating the anti-inflammatory effects of the compound in vitro and in vivo. Experiment Overall Design: Immature monocyte-derived DC were activated with anti-CD40 antibodies for 8 hours in the absence or presence of VAF347. Two donors (D1,D2) were used, resulting in four data sets: D1_ctrl, D2_ctrl (ctrl=no treatment), D1_VAF347, D2_VAF347.
2008-04-07 | E-GEOD-10463 | biostudies-arrayexpress
Project description:This study aims to elucidate the molecular mechanisms underlying the therapeutic effects of mountain-grown ginseng in allergic asthma and to systematically identify and characterize bioactive monomeric compounds responsible for these effects. We found that total saponins from mountain-grown ginseng significantly alleviated asthmatic phenotypes. Further multi-omics analyses revealed that these effects may be mediated through modulation of the arachidonic acid metabolic pathway, particularly by regulating the enzymatic activity of the rate-limiting enzyme PTGS2, thereby suppressing the production of PGE2. Subsequent component identification using high-performance liquid chromatography, combined with computational modeling, identified ginsenoside Rd2 as a key bioactive compound. In vitro cellular experiments, together with site-directed mutagenesis of the predicted binding sites, further confirmed that Rd2 exerts inhibitory effects on PTGS2 enzymatic activity through specific molecular interactions. Collectively, these findings provide mechanistic insights into the anti-asthmatic effects of mountain-grown ginseng and highlight Rd2 as a promising bioactive compound targeting PTGS2, offering potential therapeutic value for allergic asthma.
2026-04-13 | MTBLS14268 | MetaboLights
Project description:ObjectivesThis study aims to investigate the molecular mechanism by which ginsenoside Rg3 attenuates allergic asthma. Methods: This study established an ovalbumin (OVA)-induced mouse model of allergic asthma to explore the anti-allergic effects and potential molecular mechanisms of ginsenoside Rg3. The therapeutic effects of Rg3 were systematically evaluated via monitoring of general physical conditions, lung histopathological examination, inflammatory cell infiltration analysis in bronchoalveolar lavage fluid, and inflammatory cytokine detection. Furthermore, transcriptomic analyses were conducted to screen differentially expressed genes.
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Project description:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease. Lung DNA methylation profiles of mice exposed in utero to cigarette smoke (CS) then treated with house dust mite (HDM, n = 8) or saline (n = 6), or exposed in utero to filtered air (FA) then treated with HDM (n = 9) or saline (n = 6)
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