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

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

PROVIDER: PRJNA579334 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10341305.fastq.gz	Fastqsanger.gz
	SRR10341306.fastq.gz	Fastqsanger.gz
	SRR10341307.fastq.gz	Fastqsanger.gz
	SRR10341308.fastq.gz	Fastqsanger.gz
	SRR10341309.fastq.gz	Fastqsanger.gz

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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

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Interleukin-22 improves ovulation disorder via STAT3 signalling in polycystic ovary syndrome

Project description:Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disease which leads to serious impairment of reproductive health in women of child-bearing age. Anovulation or oligo-ovulation is a common clinical manifestation of PCOS patients. The disturbance of ovarian immune microenvironment contributes to the disorders of follicle development and ovulation, and the mechanism remains unclear. Here we demonstrated the protective effect of immune factor interleukin-22 (IL-22) on PCOS follicle development and ovulation. Follicular IL-22 levels were significantly lower in PCOS patients than in the control group and were positively correlated with the oocyte fertilization rate and the high-quality embryo rate. Additionally, IL-22 evidently improved follicle development in vitro and promoted ovulation-related gene expression, which was disrupted by the depletion of interleukin-22 receptor 1 (IL-22R1) or inhibition of STAT3 in granulosa cells, indicating that IL-22 acted through IL-22R1 and STAT3 signalling pathway to promote follicle development and ovulation in PCOS. In summary, this study elucidated the vital role of ovarian immune microenvironment in follicle development and ovulation, the application of IL-22 may provide new insights into the treatment of PCOS patients.

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The interleukin 22–oncostatin M axis promotes intestinal inflammation and tumorigenesis [scRNA-seq]

Project description:Multicellular cytokine networks regulate the onset of intestinal inflammation and colitis-associated cancer (CAC). Interleukin 22 (IL-22) promotes epithelial cell recovery but can also drive inflammation and tumorigenesis. We demonstrate that IL-22 from innate lymphoid cells activates STAT3 and increases OSM receptor expression in intestinal epithelial cells. This activation leads to sustained STAT3 activity via OSM, promoting inflammation and tumorigenesis. Deleting the OSM receptor or blocking OSM pharmacologically mitigates colitis and CAC. Our findings highlight the IL-22-OSM axis as a potential therapeutic target for these conditions.

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The interleukin 22–oncostatin M axis promotes intestinal inflammation and tumorigenesis [Colon_Tissue_BulkRNA-seq]

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Interleukin-22 (IL-22) regulates B3GNT7 expression to induce intestinal fucosylation of O-linked glycans

Project description:Interleukin (IL) - 22 is a cytokine that plays a critical role in the maintenance of intestinal epithelial homeostasis. Its downstream functions are mediated through ligation of its heterodimeric receptor comprised of IL-22 receptor subunit alpha 1 (IL-22Ra1) and IL-10R2, and subsequent activation of signal transducer and activator of transcription 3 (STAT3). IL-22 signaling can induce genes necessary for intestinal epithelial cell proliferation, tissue regeneration, tight junction fortification, and production of antimicrobials. Emerging studies have also implicated IL-22 signaling in the regulation of intestinal epithelial fucosylation in mice. However, whether IL-22 regulates intestinal fucosylation in human intestinal epithelial cells and the molecular mechanisms that govern this process are unknown. Here, we show that IL-22 signaling regulates expression of the B3GNT7 transcript, which encodes a β1-3-N-acetylglucosaminyltransferase that can participate in the synthesis of poly-N-acetyllactosamine (LacNAc) chains. Additionally, we show that IL-22 signaling regulates levels of the a1-3-fucosylated Lewis X (Lex) blood group antigen and this glycan epitope is primarily displayed on heavily O-glycosylated intestinal epithelial glycoproteins. The IL-22-mediated increase in Lex antigen levels requires B3GNT7, as disruption of B3GNT7 expression moderated the IL-22-dependent increase in Lex antigen levels. Moreover, we show that increased expression of B3GNT7 alone is sufficient to promote increased display of Lex-decorated carbohydrate glycan structures primarily on O-glycosylated intestinal epithelial glycoproteins. Together, the data presented here identify B3GNT7 as a critical intermediary in IL-22-dependent induction of intestinal fucosylation of O-linked glycans and uncover a novel role for B3GNT7 in intestinal glycosylation.

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2022-06-30 | GSE202314 | GEO

The interleukin 22–oncostatin M axis promotes intestinal inflammation and tumorigenesis

Project description:Multicellular cytokine networks orchestrate the onset and progression of intestinal inflammation and colitis-associated cancer (CAC). Interleukin 22 (IL-22), a member of the IL-10 superfamily, is known for promoting epithelial cell recovery but can inadvertently fuel inflammation and tumorigenesis. Here, we demonstrate that IL-22, derived from group 3 innate lymphoid cells (ILC3), triggers oncostatin M (OSM) responsiveness in intestinal epithelial cells by activating STAT3 and upregulating OSM receptor (OSMR) expression. OSM, a member of the IL-6 cytokine family implicated in inflammatory bowel disease, collaborates with IL-22 to sustain STAT3 activation, promoting proinflammatory adaptations and immune cell chemotaxis to the intestine. Conditional deletion of OSMR in epithelial cells protects mice from colitis and CAC. Additionally, pharmacological blockade of OSM reduces the progression of established CAC. Our study reveals a novel mechanism by which OSM sustains intestinal inflammation and CAC, identifying the IL-22-OSM axis as a promising therapeutic target.

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apc transcriptome-Transcriptome on Arabidopsis APC hypomorphic lines

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Interleukin-22 (IL-22) regulates B3GNT7 expression to induce intestinal fucosylation of O-linked glycans

Project description:Interleukin-22 (IL-22) regulates B3GNT7 expression to induce intestinal fucosylation of O-linked glycans

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