Ontology highlight
ABSTRACT:
PROVIDER: PRJNA534264 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8945122.fastq.gz | Fastqsanger.gz | |||
| SRR8945123.fastq.gz | Fastqsanger.gz |
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Project description:This study investigated the specific and differential gene expression in human immature DCs (iDCs) in response to treatment with a butanol fraction containing defined bioactive phytocompounds extracted from stems and leaves of Echinacea purpurea
2008-09-10 | GSE12259 | GEO
Project description:To seek scientific evidence supporting therapeutic use of Echinacea, the transcriptomic effects of Echinacea purpurea extract on mouse bone marrow-derived dendritic cells (BMDCs) were analyzed using primary cultures. Affymetrix DNA microarray and bioinformatics analyses of genes differentially expressed in DCs treated with [BF/S+L/Ep] for 4 or 12 h revealed that the majority of responsive genes were related to cell adhesion or motility (Cdh10, Itga6, Cdh1, Gja1 and Mmp8), or were chemokines (Cxcl2, Cxcl7) or signaling molecules (Nrxn1, Pkce and Acss1).
2010-09-13 | GSE19369 | GEO
Project description:Until today, natural Echinacea purpurea extracts are widely used to prevent and treat respiratory trac infections. Although its immunomodulatory effects have already been demonstrated by several studies, the molecular mechanisms involved are not yet completely understood. In this study, we applied a systems biology approach by integrating transcriptome, kinome and methylome profiles of THP-1 monocyte cells treated with Echinaforce®, a commercial standardized ethanolic tincture of Echinacea purpurea. The latter induced the expression of various genes linked to the anti-viral interferon pathway, NF-κB signaling and chemotaxis. In addition, kinase activity profiling showed that Echinaforce® increased JAK1 kinase activity, which is crucial in the activation of the JAK-STAT pathway to induce interferon-stimulated genes and MAPK kinase activity. Furthermore, gene expression changes following Echinaforce® treatment occurred largely independent from DNA methylation changes. Of special note, Echinaforce® induced global DNA hypermethylation in gene bodies, intergenic, and CpG-poor repeat regions, which could be part of an evolutionary conserved anti-viral response to suppress viral integration and/or replication. Altogether, we demonstrate that Echinaforce® treatment promotes an anti-viral response in THP-1 cells through activation of interferon, MAPK and NF-κB signaling pathways and DNA hypermethylation of repeat elements.
2019-03-31 | GSE117903 | GEO
Project description:Until today, natural Echinacea purpurea extracts are widely used to prevent and treat respiratory trac infections. Although its immunomodulatory effects have already been demonstrated by several studies, the molecular mechanisms involved are not yet completely understood. In this study, we applied a systems biology approach by integrating transcriptome, kinome and methylome profiles of THP-1 monocyte cells treated with Echinaforce®, a commercial standardized ethanolic tincture of Echinacea purpurea. The latter induced the expression of various genes linked to the anti-viral interferon pathway, NF-κB signaling and chemotaxis. In addition, kinase activity profiling showed that Echinaforce® increased JAK1 kinase activity, which is crucial in the activation of the JAK-STAT pathway to induce interferon-stimulated genes and MAPK kinase activity. Furthermore, gene expression changes following Echinaforce® treatment occurred largely independent from DNA methylation changes. Of special note, Echinaforce® induced global DNA hypermethylation in gene bodies, intergenic, and CpG-poor repeat regions, which could be part of an evolutionary conserved anti-viral response to suppress viral integration and/or replication. Altogether, we demonstrate that Echinaforce® treatment promotes an anti-viral response in THP-1 cells through activation of interferon, MAPK and NF-κB signaling pathways and DNA hypermethylation of repeat elements.
2019-03-31 | GSE117902 | GEO
Project description:Echinacea, native to the Canadian prairies and the prairie states of the United States, has a long tradition as a folk medicine for the Native Americans. Currently, Echinacea are among the top 10 selling herbal medicines in the U.S. and Europe, due to increasing popularity for the treatment of common cold and ability to stimulate the immune system. However, the genetic relationships within the species of this genus are unclear, which makes difficult the authentication of the species used for the medicinal industry. We report the construction of a novel Subtracted Diversity Array (SDA) for Echinacea species and demonstrate the potential of this array for isolating highly polymorphic sequences. In order to selectively isolate Echinacea-specific sequences, a Suppression Subtractive Hybridization (SSH) was performed between a pool of twenty-four Echinacea genotypes and a pool of other angiosperms and non-angiosperms. A total of 283 subtracted genomic DNA (gDNA) fragments were amplified and arrayed. Twenty-seven Echinacea genotypes, including four that were not used in the array construction, could be successfully discriminated. Interestingly, unknown samples of E. paradoxa and E. purpurea could be unambiguously identified from the cluster analysis. Furthermore, this Echinacea-specific SDA was also able to isolate highly polymorphic sequences. Five out of the eleven most discriminatory features matched to known retrotransposons.
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Project description:To seek scientific evidence supporting therapeutic use of Echinacea, the transcriptomic effects of Echinacea purpurea extract on mouse bone marrow-derived dendritic cells (BMDCs) were analyzed using primary cultures. Affymetrix DNA microarray and bioinformatics analyses of genes differentially expressed in DCs treated with [BF/S+L/Ep] for 4 or 12 h revealed that the majority of responsive genes were related to cell adhesion or motility (Cdh10, Itga6, Cdh1, Gja1 and Mmp8), or were chemokines (Cxcl2, Cxcl7) or signaling molecules (Nrxn1, Pkce and Acss1). Experiment Overall Design: BMDCs from mice were treated with [BF/S+L/Ep] or DMSO for 4 h or 12 h in duplicates.
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