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Regulation of gene expression in enteroids by butyrate and IL-13

ABSTRACT: Regulation of gene expression in enteroids by butyrate and IL-13

PROVIDER: PRJNA928469 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23248084_1.fastq.gz	Fastqsanger.gz
	SRR23248084_2.fastq.gz	Fastqsanger.gz
	SRR23248085_1.fastq.gz	Fastqsanger.gz
	SRR23248085_2.fastq.gz	Fastqsanger.gz
	SRR23248086_1.fastq.gz	Fastqsanger.gz

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Regulation of gene expression in enteroids by butyrate and IL-13

Project description:Expression in organoids dervied from the ileum of WT C57Bl/6 mice stimulated with butyrate, IL-13, or butyrate + IL-13. Intestinal organoids were stimulated with butyrate for 48hrs, then IL-13 for 72 hrs. RNA was isolated using RNeasy Kit (Qiagen). Sequencing was performed using the Illumina HiSeq2500. Reads were mapped to the mm10 genome using Bowtie.

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single-cell RNA sequencing for enteroids treated with IL-17

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The Role of Butyrate as a Histone Deacetylase Inhibitor in Protecting Pancreatic Beta Cells from IL-1β-Induced Dysfunction

Project description:Butyrate, a gut microbial metabolite, has beneficial effects on glucose homeostasis and has become an attractive drug target for type 2 diabetes (T2D). Recently, we showed that butyrate protects pancreatic beta cells against cytokine-induced dysfunction. In this study, we explored the underlying mechanisms of butyrate action. Pancreatic islets were exposed to a non-cytotoxic concentration of interleukin 1β (IL-1β) for ten days to mimic the low-grade inflammation in T2D. An isoform-selective histone deacetylase 3 (HDAC3) inhibitor normalized IL-1β-reduced GSIS and insulin content similar to the effect of butyrate. In contrast, FFAR2/3 agonists failed to normalize IL-1β-induced impairment of GSIS and reduced insulin content. Butyrate, irrespective of IL-1β, inhibited HDAC activity and increased histone H3 and H4 acetylation by 3- and 10-fold, respectively. Genome-wide analysis of histone H3K27 acetylation (H3K27ac) revealed that butyrate mainly increased H3K27ac at promoter regions (~68 %), while H3K27ac peaks regulated by IL-1β were more equally distributed at promoters (~33 %), introns (~23 %) and intergenic regions (~23 %). Gene ontology analysis showed that butyrate increased IL-1β-reduced H3K27ac levels near several genes related to hormone secretion and reduced IL-1β-increased H3K27ac levels near genes associated with inflammatory responses . Butyrate alone increased H3K27ac near many genes related to MAPK signaling, hormone secretion and differentiation, and decreased H3K27ac at genes involved in cell replication. Together, these results suggest that butyrate prevents IL-1β-induced beta cell dysfunction by inhibition of HDACs resulting in changes in H3K27ac levels at genes relevant for beta cell function and inflammatory responses.

2023-12-07 | GSE233936 | GEO

Whole Lung Proteome in N. brasiliensis Infection in IL-13 deficient mice.

Project description:IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of allergic and fibrotic diseases. Matrix remodelling is an important component of repair processes in the lung but is also a hallmark of chronic diseases such as asthma. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these two type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 in more acute settings of tissue injury/repair and whether IL-13 regulates remodelling of the extracellular matrix following tissue injury. In this study, we used Nippostrongylus brasiliensis infection as model of acute lung tissue damage and repair by comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.

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Project description:Myelofibrosis (MF) is a disease with high unmet medical need since bone marrow transplant is not an option for many patients and JAK inhibitors are generally effective for only 2-3 years. MF is characterized by the presence of dysplastic megakaryocytes and progression to fulminant disease is associated with significantly increased fibrosis in the bone marrow. Despite evidence of an inflammatory state in MF that drives disease progression, the specific factors that promote megakaryocyte growth are poorly understood. Here, we analyzed changes in the cytokine profiles of MF mouse models before and after development of fibrosis coupled with analysis of bone marrow populations by scRNA-seq. We found high IL-13 levels in the bone marrow of MF mice. IL-13 promoted the growth of mutant megakaryocytes and induced the surface expression of TGF-B and collagen biosynthesis. Analysis of samples from patients with myelofibrosis revealed elevated levels of IL-13 in plasma and increased IL-13 receptor expression in megakaryocytes in the bone marrow, indicating that our observations in mice are relevant in human disease. In vivo, IL-13 overexpression promoted disease progression while reducing IL-13/IL-4 signaling reduced several features of the disease including fibrosis. Lastly, we found an increase in T cells and mast cells, which are known sources of IL-13 in MF bone marrow. Together, our data demonstrate that IL-13 is involved in the progression of MF and that inhibition of the IL-13/IL-4 signaling pathway should be investigated as a therapeutic option in MF.

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RNA sequencing for enteroids treated with different concentrations of IL-17 (0 ng/ml. 1 ng/ml, 10 ng/ml and 100 ng/ml)

Project description:To evaluate the intestinal epithelial responses induced by IL-17, bulk RNA-sequencing (RNA-seq) was performed on the human small intestinal organoids (enteroids, n = 3) treated with different concentrations of IL-17 (0 ng/ml. 1 ng/ml, 10 ng/ml and 100 ng/ml) .

2021-08-20 | GSE182453 | GEO

single-cell RNA sequencing for enteroids treated with IL-17

Project description:single-cell RNA sequencing for enteroids treated with IL-17

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