Ontology highlight
ABSTRACT:
PROVIDER: PRJNA848096 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19628000_1.fastq.gz | Fastqsanger.gz | |||
| SRR19628000_2.fastq.gz | Fastqsanger.gz | |||
| SRR19628001_1.fastq.gz | Fastqsanger.gz | |||
| SRR19628001_2.fastq.gz | Fastqsanger.gz | |||
| SRR19628002_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Inflammatory Bowel Disease (IBD) is a term describing a collection of conditions characterised by chronic inflammatory disorder of the gastrointestinal tract involving an inappropriate immune response to commensal microorganisms in a genetically susceptible host. Four kiwifruit extracts, aqueous and ethyl acetate extracts of gold kiwifruit (Actinidia chinensis) or green kiwifruit (A. deliciosa), have previously demonstrated anti-inflammatory activity using in vitro models of IBD. This study examined whether these kiwifruit extracts had immune modulating effects in vivo against inflammatory processes known to be increased in patients with IBD. KFEs were used as a dietary intervention in Il10-/- mice (an in vivo model of IBD) and the C57BL/6J background strain in a 3 x 2 factorial design. While all Il10-/- mice developed significant colonic inflammation compared to the C57BL/6J mice, this was not affected by the inclusion of KFE in the diet. Whole genome gene and protein expression level profiling indicated that KFEs influenced immune signalling pathways and metabolic processes within the colonic tissue; however, the effects were subtle. In particular, adaptive immune pathways were reduced by three out of four kiwifruit extracts, with greater reduction seen in the C57BL/6J mice. This suggests that while immune-modulating activity was present in vivo, KFEs did not reduce inflammatory processes relevant to IBD. Experimental design. Two experiments were conducted, one using extracts from gold kiwifruit and one using extracts from green kiwifruit. Within each experiment, both Il10-/- and C57 mice were randomly divided into three diet treatment groups, to ive the following 12 treatments: 1) Gold Kiwifruit Experiment, C57BL/6J mice, Control diet (AIN-76A), 2) Gold Kiwifruit Experiment, C57BL/6J mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 3) Gold Kiwifruit Experiment, C57BL/6J mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) 4) Gold Kiwifruit Experiment, Il10-/- mice, Control diet (AIN-76A), 5) Gold Kiwifruit Experiment, Il10-/- mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 6) Gold Kiwifruit Experiment, Il10-/- mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) 7) Green Kiwifruit Experiment, C57BL/6J mice, Control diet (AIN-76A), 8) Green Kiwifruit Experiment, C57BL/6J mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 9) Green Kiwifruit Experiment, C57BL/6J mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) 10) Green Kiwifruit Experiment, Il10-/- mice, Control diet (AIN-76A), 11) Green Kiwifruit Experiment, Il10-/- mice, Aqueous Kiwifruit Extract Supplemented Diet (AIN-76A + 5% Aqueous KFE) 12) Green Kiwifruit Experiment, Il10-/- mice, Ethyl Acetate Kiwifruit Extract Supplemented Diet (AIN-76A + 0.11% Ethyl Acetate KFE) Six biological replicates were analysed from each treatment group, except for groups 3 and 7 where five replicates were analysed due to array quality issues with the sixth replicate. Each replicate contained mRNA from one mouse. A reference design was used, where each slide was hybridised with mRNA from one sample (green channel) and mRNA from a common reference pool (red channel).
2011-03-05 | E-GEOD-27684 | biostudies-arrayexpress
Project description:Genome-wide analysis of H3K4me3 and Ikaros profiles in fresh or frozen mouse splenic B cells via CUT&RUN
2021-09-07 | GSE172130 | GEO
Project description:Inflammatory Bowel Disease (IBD) is a term describing a collection of conditions characterised by chronic inflammatory disorder of the gastrointestinal tract involving an inappropriate immune response to commensal microorganisms in a genetically susceptible host. Four kiwifruit extracts, aqueous and ethyl acetate extracts of gold kiwifruit (Actinidia chinensis) or green kiwifruit (A. deliciosa), have previously demonstrated anti-inflammatory activity using in vitro models of IBD. This study examined whether these kiwifruit extracts had immune modulating effects in vivo against inflammatory processes known to be increased in patients with IBD. KFEs were used as a dietary intervention in Il10-/- mice (an in vivo model of IBD) and the C57BL/6J background strain in a 3 x 2 factorial design. While all Il10-/- mice developed significant colonic inflammation compared to the C57BL/6J mice, this was not affected by the inclusion of KFE in the diet. Whole genome gene and protein expression level profiling indicated that KFEs influenced immune signalling pathways and metabolic processes within the colonic tissue; however, the effects were subtle. In particular, adaptive immune pathways were reduced by three out of four kiwifruit extracts, with greater reduction seen in the C57BL/6J mice. This suggests that while immune-modulating activity was present in vivo, KFEs did not reduce inflammatory processes relevant to IBD. SUBMITTER_CITATION: Edmunds, Shelley Jane. The effects of kiwifruit extracts on gene and protein expression in in vitro and in vivo mouse models of inflammatory bowel disease. Diss. University of Auckland, New Zealand, 2010. http://hdl.handle.net/2292/6623
2011-03-05 | GSE27684 | GEO
Project description:In the present study, an iTRAQ-based quantitative proteomic analysis, combined with gene expression and virus-induced gene silencing (VIGS), were used to identify genes associated with the infection of kiwifruit (Actinidia deliciosa ‘Hayward’) by B. cinerea. To the best of our knowledge, this is the first proteomic study of the kiwifruit-B. cinerea interaction, and provides information that can be used to better understand the mechanism of gray mold infection in kiwifruit.
2018-03-05 | PXD008589 | Pride
Project description:Kiwifruit bacterial canker caused by Pseudomonas syringae pv. actinidiae (Psa) is the emerging global concern for kiwifruit production. The successful infection of Psa in kiwifruit relies on the type III secretion system (T3SS), and its regulatory pathway is modulated by hrpR/S-L. However, the mechanisms by which certain transcriptional factors regulate this pathway remain less understood. In this study, we have identified the TetR/AcrR family transcription factor (TF) C_22735 in the Psa3-M228 strain through both Tn libraries and DNA pull-down strategy. The genetic mutation in TF C_Δ22735 exhibited a significantly decreased pathogenicity, and showed diminished ability to induce a hrpR/S/L and hrpA expression in kiwifruit leaves, and twigs, as well as reduced hypersensitive response (HR) in Nicotiana benthamiana. Similarly, another gene C_04700 knockout strain capacity to induce tobacco HR, and its pathogenicity to kiwifruit leaf discs was also significantly reduced. Moreover, the considerable overlap in down-regulated genes between Δ22735 and Δ4700 mutants highlights the intertwined regulatory roles of C_22735 and C_04700, and it suggests a tightly coordinated regulatory system, where C_04700 may serve as a primary signal sensor and C_22735 as a downstream transcriptional activator. In addition, Transcriptomic studies and, electrophoretic mobility shift assays (EMSA), and fluorescence detection indicated that C_22735 not only positively regulates T3SS but also directly binds to the upstream untranslated regions of hrpR/S and hrpL to modulate T3SS activity. This is the first study revealing the insights into TF C_22735 regulating virulence of Psa, which additively require TCS. This study adds up a novel pathway of T3SS regulation and provide the foundation for further research.
2025-01-31 | GSE286487 | GEO
Project description:Transcriptome analysis in fresh-cut cabbage during storage
| PRJDB7619 | ENA