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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

ABSTRACT: We found IL22 could reduce intestinal fatty acid transporters expression. We used single cell RNA sequencing (scRNA-seq) to analyze the cell population and gene expression with Fc or IL-22Fc treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE242927 | GEO | 2024/08/01

REPOSITORIES: GEO

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

Project description:IL22 induces antimicrobial peptides which influnce microbiota. We used 16s rRNA gene sequencing (16s DNA-seq) to analyze the microbiota with Fc or IL-22Fc treatment.

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [scRNA-seq]

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IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

Project description:IL-22 resolves MASLD via enterocyte STAT3 restoration of diet perturbed intestinal homeostasis [16s rDNA-seq]

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Rehydration rescues Il22-/- mice from lethal Citrobacter rodentium infection

Project description:Interleukin-22 (IL-22) is considered indispensable for host defence against Citrobacter rodentium (CR), with 100% mortality of Il22-/- mice post infection. While IL-22 promotes epithelial barrier integrity and antimicrobial peptide production, the precise mechanism underlying Il22-/- lethality remains unclear. Here, we show that Il22-/- mice succumb to CR infection due to dehydration rather than uncontrolled bacterial burden or inability to regenerate intestinal epithelium. Proteomic analysis at 9 days post infection (dpi) revealed significant downregulation of ion transporters (Slc26a3, Aqp8, Ca2, Ca4, Slc5a8, Pept1) in Il22-/- colonic epithelial cells, suggesting an association between IL-22 deficiency and impaired fluid-electrolyte balance. Fluid therapy (FT), initiated at 5 dpi and lasted for 2 weeks, fully rescued Il22-/- mice, restoring survival without reducing bacterial burden, or affecting immune responses or epithelial integrity. Recovered Il22-/- mice exhibited epithelial regeneration and protection against reinfection, demonstrating that IL-22-independent pathways support long-term mucosal recovery. Notably, advanced AI models consistently failed to predict IL-22’s dispensability. These findings overturn the long-standing paradigm that IL-22 is indispensable for recovery from enteric infection, suggesting that alternative mechanisms can drive epithelial repair and host recovery.

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A20’s Linear Ubiquitin Binding Motif Restrains Pathogenic Activation of TH17/22 cells and IL-22 Driven Enteritis [scRNA-seq]

Project description:A20, encoded by the TNFAIP3 gene, is a protein linked to Crohn and celiac disease in humans. We show that mice expressing point mutations in A20’s M1-ubiquitin binding zinc-finger 7 (ZF7) domain spontaneously develop proximal enteritis that requires both luminal microbes and T cells. Cellular and transcriptomic profiling reveal expansion of TH17/22 cells and exuberant expression of IL-17A and IL-22 in intestinal lamina propria of A20ZF7 mice. While deletion of IL-17A from A20ZF7 mice exacerbates enteritis, deletion of IL-22 abrogates intestinal epithelial cell hyperproliferation, barrier dysfunction, and alarmin expression. Colonization of adult germ-free mice with normal luminal flora drives duodenal IL-22 expression and duodenitis. A20ZF7 TH17/22 cells autonomously express more RORgammat and IL-22 after differentiation in vitro. ATAC sequencing identified an enhancer region upstream of the Il22 gene, and this enhancer demonstrated increased activating histone acetylation coupled with exaggerated Il22 transcription in A20ZF7 T cells. Acute inhibition of RORgammat normalized histone acetylation at this enhancer. Finally, CRISPR/Cas9-mediated ablation of A20ZF7 in human T cells increases RORgammat expression and IL22 transcription. These studies link A20’s M1-ubiquitin binding function with RORgammat expression, expansion of TH17/22 cells, and epigenetic activation of IL-22 driven enteritis.

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A20’s Linear Ubiquitin Binding Motif Restrains Pathogenic Activation of TH17/22 cells and IL-22 Driven Enteritis [RNA-Seq]

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