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RNA-seq of small intestinal organoids treated with IL-22 for 0, 1 and 4 hours

ABSTRACT: RNA-seq of small intestinal organoids treated with IL-22 for 0, 1 and 4 hours

PROVIDER: PRJEB49518 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR7756041_1.fastq.gz	Fastqsanger.gz
	ERR7756041_2.fastq.gz	Fastqsanger.gz
	ERR7756042_1.fastq.gz	Fastqsanger.gz
	ERR7756042_2.fastq.gz	Fastqsanger.gz
	ERR7756043_1.fastq.gz	Fastqsanger.gz

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RNAseq of small intestinal organoids from mice treated with the cytokines IFNG, IL-13 and IL-22 for 24 hours

Project description:The intestinal epithelium is our first line of defense against infections of the gut and the plasticity in cellular differentiation of the intestinal epithelium is an important part of this response. The changes in cellular composition is driven by immune cell derived cytokines. Here we use signature cytokines of different type of immune responses applied to small intestinal organoids to model how different immune responses affect intestinal epithelial development. Simplified, IFNG represents type I immunity against intracellular pathogens such as viruses, IL-13 represents type II immunity against infections such as parasites and IL-22 represents type III immunity against extracellular bacterial infections. To not influence organoid formation, organoids were grown 24 hours without cytokines, and then 10 ng/mL of cytokine was applied for 24 hours before harvesting RNA. Furthermore, IFNG is supplied in combination with the other cytokines as cytokines are rarely found alone in an inflammation setting. We find that these cytokines affect developmental pathways of the intestinal epithelium and affect the cellular composition of the intestinal epithelium.

2022-05-08 | E-MTAB-9182 | biostudies-arrayexpress

RNAseq of small intestinal organoids from mice treated with the cytokines IL-13 and IL-22 for 72 hours in combination with the BMP signaling inhibitor DMH1

Project description:The intestinal epithelium is our first line of defense against infections of the gut and the plasticity in cellular differentiation of the intestinal epithelium is an important part of this response. The changes in cellular composition is driven by immune cell derived cytokines. Here we use signature cytokines of different type of immune responses applied to small intestinal organoids to model how different immune responses affect intestinal epithelial development. Simplified, IL-13 represents type II immunity against infections such as parasites and IL-22 represents type III immunity against infections such as extracellular bacterial infections. 10 ng/mL of IL-13 and IL-22 was added for 72 hours after splitting. Furthermore, we have found BMP signaling to be important in regulating the cellular differentiation induced by IL-13. We therefore added added a combination treatment with the activin receptor-like kinase 2 (ALK-2) signaling inhibitor Dorsomorphin homolog 1 (DMH1) in concentration of 5 uM. We find that ALK-2 signaling is crucial for IL-13 driven Tuft cell differentiation.

2022-05-08 | E-MTAB-9185 | biostudies-arrayexpress

RNA-seq of small intestinal organoids treated with IL-22 for 0, 1 and 4 hours

Project description:The intestinal epithelium is our first line of defence against infections of the gut and the plasticity in cellular differentiation of the intestinal epithelium is an important part of this response. The changes in cellular composition is driven by immune cell derived cytokines. Here we investigate the response over time upon stimulation with 10 ng/mL of the cytokine Interleukin-22 (IL-22).

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Investigating the Interleukin-22 regulated transcriptome in normal and APC-mutant small intestinal epithelial organoids

Project description:Purpose: to investigate the effects of the cytokine Interluekin-22 (IL-22) on small intestinal epithelial cells, using organoids. Methods: WT or Apc(Min/Min) organoids (day 3) were stimulated with IL-22 (2ng/ml) for 3 hours, and submitted for transcriptomic profiling. Results: The main function of IL-22 in small intestinal epithelial cells is to activate an antimicrobial immune response and defence against infection and stress. Further, we found that loss of Apc lead to a complete loss of response to IL-22

2019-10-25 | GSE139332 | GEO

Tifa-/- vs Tifa+/+ small intestinal organoids stimulated with water, IL-22, IL-22+ADP-Heptose

Project description:Tifa-/- vs Tifa+/+ small intestinal organoids stimulated with water, IL-22, IL-22+ADP-Heptose

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RNAseq of small intestinal organoids from mice treated with the cytokines IFNG, IL-13 and IL-22 for 24 hours

Project description:RNAseq of small intestinal organoids from mice treated with the cytokines IFNG, IL-13 and IL-22 for 24 hours

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Expression data from keratinocytes treated either with IL-22 or combination of tofacitinib (JAK1/3 inhibitor) and IL-22 at 6 hours

Project description:JAK inhibitors like tofacitinib were thought to act primarily on T cells. However, our data and recent research suggest that JAK receptors are also present on keratinocytes. Here, we show effect of tofacitinib on primary keratinocytes, which could explain effects of topical tofacitinib treatment in psoriasis. We have performed whole transcriptome analysis (using microarray) on RNA isolated from cultured primary keratinocytes treated either with IL-22 alone or combination of tofacitinb and IL-22 at 6 hours

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Expression data from keratinocytes treated either with IL-22 or combination of tofacitinib (JAK1/3 inhibitor) and IL-22 at 6 hours

Project description:Expression data from keratinocytes treated either with IL-22 or combination of tofacitinib (JAK1/3 inhibitor) and IL-22 at 6 hours

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RNA-seq of small intestinal organoids treated with IL-13 for 0, 1, 4 8 and 24 hours and with the BMP signaling inhibitor DMH1

Project description:The intestinal epithelium is our first line of defense against infections of the gut and the plasticity in cellular differentiation of the intestinal epithelium is an important part of this response. The changes in cellular composition is driven by immune cell derived cytokines. Here we investigate the response over time upon stimulation with 10 ng/mL of the cytokine Interleukin-13 (IL-13). The intestinal organoids were lyzed 48 hours after splitting and IL-13 was added 24h, 8h, 4h and 1h before lysis. Furthermore, we have found BMP signaling to be important in regulating the cellular differentiation induced by IL-13. We therefore added added a combination treatment with the activin receptor-like kinase 2 (ALK-2) signaling inhibitor Dorsomorphin homolog 1 (DMH1) in concentration of 5 uM in some samples 24 hours before lysis. We find that ALK-2 signaling is crucial for IL-13 driven Tuft cell differentiation.

2022-05-08 | E-MTAB-10455 | biostudies-arrayexpress

IL-22 promotes cell proliferation to combat virus infection in human intestinal epithelial cells

Project description:Interferon lambdas (IFN-λs) are crucial to control virus infections at mucosal surfaces. Interleukin-22 (IL-22) was reported to help IFN-λ control rotavirus infection in mice either by aiding in the induction of interferon stimulated genes (ISGs) or by increasing cell proliferation thereby clearing virally infected cells. We investigated whether IL-22 and IFN-λs exhibited similar synergistic effects in human intestinal epithelial cells models. Our results showed that co-treatment of IL-22 and IFN-λ induced more phosphorylation of STAT1 than either cytokine used alone. However, this increased STAT1 activation did not translate to increased ISG production or antiviral protection. Transcriptomics analysis revealed that despite sharing a receptor and activating the similar STATs, the signaling generated by IL-22 and IFN-λs is independent where IFN-λs signaling induces ISGs and IL-22 signaling induces cell proliferation genes. Using human intestinal organoids, we confirmed that IL-22 increased the size of the organoids due to increased cell proliferation and increasing the stem cell marker (OLFM4). These findings suggest that in human intestinal cells, IFN-λs and IL-22 act independently to clear virus infections. IFN-λs induce ISGs to control virus replication and spread while IL-22 increases cell proliferation to eliminate infected cells and repair the damage epithelium. Although, these two cytokines do not increase each other’s function, they each play a key role in protecting human intestinal epithelium cells.

2023-12-30 | GSE243230 | GEO

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