Ontology highlight
ABSTRACT:
PROVIDER: PRJNA669121 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12833050.fastq.gz | Fastqsanger.gz | |||
| SRR12833051.fastq.gz | Fastqsanger.gz | |||
| SRR12833052.fastq.gz | Fastqsanger.gz | |||
| SRR12833053.fastq.gz | Fastqsanger.gz | |||
| SRR12833054.fastq.gz | Fastqsanger.gz |
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Project description:TFEB in IEC has a protective role in DSS colitis. The goal is to examine what genes/pathways are TFEB target during DSS colitis
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Project description:Inflammatory bowel disease (IBD), comprising Crohn´s disease and Ulcerative colitis, is characterized by chronic relapsing inflammation of the gut. It has been shown that increased proteasomal activity is associated with the expression of immunoproteasomes, which enhances NF-kB activation and thus promotes inflammation in IBD-patients. Here, we investigate whether modulation of the proteasomal activity is a suitable therapeutic approach to limit inflammation in colitis. This concept was tested in two different experimental setups. First, development of dextran sulfate sodium (DSS)-induced colitis was tested in lmp7-/--mice, which lack the essential immunoproteasome-subunit LMP7 or in wildtype-mice treated with the proteasome inhibitor bortezomib. Compared to WT mice, lmp7-/- mice revealed significantly attenuated colitis resulting from reduced NF-kB activation in the absence of LMP7. Further, treatment with bortezomib revealed dose-dependent amelioration of DSS-induced inflammation. In both approaches proteasome modulation limited the infiltration of neutrophils, consequently reducing tissue damage. In summary our experiments demonstrate that modulation of the proteasomal activity is effective in attenuating experimental colitis. In particular, our data suggest that the immunoproteasome-subunit LMP7 is a suitable target for the therapy of IBD.
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Project description:Ulcerative colitis (UC) is a chronic inflammatory condition of the colon, characterized by recurring mucosal inflammation. Current evidence suggests that dysbiosis may drive the disease, but mechanistic links remain incompletely understood. To further investigate the host-microbiome interactions, three UC-induction methods were used on a pseudo germ-free mouse model: (1) DSS, (2) fecal microbiota transplantation (FMT) from a UC patient, and (3) combination of both DSS and FMT simultaneously. Disease severity (DAI), immune cell profiles (flow cytometry), colon transcriptomics (RNA sequencing), and microbiota composition (16S rRNA sequencing) were assessed. Our study revealed distinct effects of DSS and FMT on experimental colitis. DSS had a more pronounced impact on disease severity, while FMT exerted a stronger influence on several immune populations and downregulation of genes associated with tight junctions and mucins. Microbiome analysis demonstrated distinct compositional profiles across all experimental groups. The combined FMT and DSS model exhibited features of both induction methods, resulting in exacerbated clinical scores, barrier dysfunction, and inflammatory responses. Our study provides valuable insight into host–microbiome interactions in UC and introduces a dual-hit approach that may more accurately recapitulate its multifactorial pathogenesis than DSS alone.
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Project description:Poly(ADP-ribose) polymerases (PARPs) synthesize and bind branched polymers of ADP-ribose to acceptor proteins using NAD as a substrate, and participate to the control of gene transcription and DNA repair. PARP1, the most abundant isoform, regulates the expression of proinflammatory mediator - cytokines, chemokines and adhesion molecules, and inhibition of PARP1 enzymatic activity reduced or ameliorated autoimmune diseases in several experimental models, including colitis. However, the mechanism(s) underlying the protective effects of PARP1 inhibition in colitis and the cell types in which Parp1 deletion has the most significant impact are unknown. The objective of the current study was to determine the impact of Parp1 deletion on the innate immune response to mucosal injury. Genome-wide analysis of the colonic transcriptome was performed. Compared to WT, we demonstrated that Parp1-/-were protected from DSS-induced colitis and that this protection was associated with a dramatic transcriptional reprogramming in the colon. WT or Parp1-/- mice were treated with drinking water administered ad libitum without ot with 4% dextran sulfate (DSS) for seven days. Whole colon was collected for RNA extraction and hybridization on Affymetrix microarrays. Thee mice from each genotype/treatment groups were used in the analysis.
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Project description:Inflammatory bowel disease (IBD), comprising CrohnM-BM-4s disease and Ulcerative colitis, is characterized by chronic relapsing inflammation of the gut. It has been shown that increased proteasomal activity is associated with the expression of immunoproteasomes, which enhances NF-kB activation and thus promotes inflammation in IBD-patients. Here, we investigate whether modulation of the proteasomal activity is a suitable therapeutic approach to limit inflammation in colitis. This concept was tested in two different experimental setups. First, development of dextran sulfate sodium (DSS)-induced colitis was tested in lmp7-/--mice, which lack the essential immunoproteasome-subunit LMP7 or in wildtype-mice treated with the proteasome inhibitor bortezomib. Compared to WT mice, lmp7-/- mice revealed significantly attenuated colitis resulting from reduced NF-kB activation in the absence of LMP7. Further, treatment with bortezomib revealed dose-dependent amelioration of DSS-induced inflammation. In both approaches proteasome modulation limited the infiltration of neutrophils, consequently reducing tissue damage. In summary our experiments demonstrate that modulation of the proteasomal activity is effective in attenuating experimental colitis. In particular, our data suggest that the immunoproteasome-subunit LMP7 is a suitable target for the therapy of IBD. Microarray experiments were performed as dual-color hybridizations. To compensate for dye-specific effects, a dye-reversal color-swap was applied. Samples of proximal colon were cut longitudinally, washed in PBS, shortly incubated in 4M Guanidinium-isothiocyanat and transferred to TRIzol (Invitrogen).
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