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E-MTAB-9182

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

PROVIDER: E-MTAB-9182 | ExpressionAtlas | 2023-06-16

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-MTAB-9182-analysis-methods.tsv	Tabular
	E-MTAB-9182-analytics.tsv	Tabular
	E-MTAB-9182-apply_fixes_zooma_mappings.done	Other
	E-MTAB-9182-atlasExperimentSummary.Rdata	Rdata
	E-MTAB-9182-configuration.xml	Xml

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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

| PRJEB38674 | ENA

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

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

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

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: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

| PRJEB38684 | ENA

RNAseq of small intestinal epithelium extracted from mice infected with Nippostrongylus brasiliensis

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. Here we sequenced the small intestinal epithelium from mice infected with Nippostrongylus brasiliensis to determine how the intestinal epithelium adapts in the context of an infection. By comparing these data to small intestinal organoids treated with cytokines (see related accessions) we determine that the intestinal epithelial response to N. brasiliensis infection correspond to a type II infection driven by IL-13.

2022-05-08 | E-MTAB-9183 | 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

ILC3s-derived RANKL contributes to tuft cell hyperplasia and anti-helminth immunity

Project description:Intestinal tuft cells are reported to orchestrate parasite type 2 immunity through producing IL-25 and LTC4. Meanwhile, type 2 cytokines IL-13 and IL-4 can induce tuft cell hyperplasia from intestinal stem cells during helminth infection. Here, using intestinal organoids culture, we show that RANKL synergizes with both IL-13 and IL-4 to enhance tuft cell expansion. Genetic mouse models revealed that RANK-RelB axis in intestinal epithelial cells (IECs) is required for optimal tuft cell-ILC2 circuit activation during helminth infection. Mechanistically, RANKL enhances IL-13-activated IL-4RA/STAT6 signaling in IECs, promoting tuft cell differentiation. Using genetic mouse models, we further demonstrated that ILC3s-derived RANKL is indispensable for optimal tuft cell hyperplasia during helminth infection. The scRNA-seq data revealed that N. brasiliensis infection will modulate ILC3 subsets distribution and RANKL expression.

2025-05-19 | GSE247660 | GEO

Optimal human intestinal organoid model reveals interleukin-22-induced Paneth cell differentiation

Project description:Here, we developed an optimal system for culturing human small intestinal organoids (hSIOs) that recapitulate the structural and functional complexity of the intestinal crypt in vitro, including mature Paneth cells. With this model, we found that IL-22 is required for the differentiation of human Paneth cells. Rather than STAT3, the PI3K-mTORC1 axis, downstream of IL-22, mediates Paneth cell differentiation programs. CD-associated variants of the IL-22 receptor (IL10RB) were introduced in our system, resulting in the abolishment of Paneth cells in hSIOs. Moreover, our data demonstrated that long-term IL-22 exposure inhibited the growth of hSIOs, challenging the current perception of IL-22 in promoting intestinal regeneration, but rather in reducing cell viability. As a proof-of-principle, our study demonstrates that this optimal culture system for hSIOs has great potential for modelling human intestinal physiology and pathophysiology.

2022-08-23 | GSE189423 | GEO

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