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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE195607 | GEO | 2022/01/31

REPOSITORIES: GEO

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Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [scRNAseq_Treg]

Project description:Iron deficiencies are the most common non-enteric syndromes observed in patients with inflammatory bowel diseases (IBD), yet little is known how iron deficiencies impact immune tolerance in the intestine. The goal of this study is to illuminate role of iron in colonic Treg homeostasis regulation.

2022-01-31 | GSE195604 | GEO

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [Treg_in_vivo]

2022-01-31 | GSE195603 | GEO

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]

2022-01-31 | GSE195602 | GEO

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine.

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine.

| PRJNA801469 | ENA

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [scRNAseq_Treg]

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [scRNAseq_Treg]

| PRJNA801476 | ENA

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [Treg_in_vivo]

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [Treg_in_vivo]

| PRJNA801477 | ENA

Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]

Project description:Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]

| PRJNA801478 | ENA

Microbiota-assisted iron uptake promotes immune tolerance in the intestine.

Project description:Iron deficiencies are the most common nonenteric syndromes observed in patients with inflammatory bowel disease, but little is known about their impacts on immune tolerance. Here we show that homeostasis of regulatory T cells in the intestine was dependent on high cellular iron levels, which were fostered by pentanoate, a short-chain fatty acid produced by intestinal microbiota. Iron deficiencies in Treg caused by the depletion of Transferrin receptor 1, a major iron transporter, result in the abrogation of Treg in the intestine and lethal autoimmune disease. Transferrin receptor 1 is required for differentiation of c-Maf+ Treg, major constituents of intestinal Treg. Mechanistically, iron enhances the translation of HIF-2α mRNA, and HIF-2α in turn induces c-Maf expression. Importantly, microbiota-produced pentanoate promotes iron uptake and Treg differentiation in the intestine. This subsequently restores immune tolerance and ameliorated iron deficiencies in mice with colitis. Our results thus reveal an association between nutrient uptake and immune tolerance in the intestine.

| S-EPMC10185671 | biostudies-literature

Strigolactones are involved in enhancing iron uptake in maize

Project description:A whole transcriptome (RNA-seq) study of maize root and shoots under iron sufficient, deficient and resupply conditions was carried out to determine the genes that are iron-regulated in the roots and shoots.

2024-10-30 | GSE280702 | GEO

Prostaglandin E2 promotes intestinal inflammation via inhibiting microbiota-dependent regulatory T cells.

Project description:The gut microbiota fundamentally regulates intestinal homeostasis and disease partially through mechanisms that involve modulation of regulatory T cells (Tregs), yet how the microbiota-Treg cross-talk is physiologically controlled is incompletely defined. Here, we report that prostaglandin E2 (PGE2), a well-known mediator of inflammation, inhibits mucosal Tregs in a manner depending on the gut microbiota. PGE2 through its receptor EP4 diminishes Treg-favorable commensal microbiota. Transfer of the gut microbiota that was modified by PGE2-EP4 signaling modulates mucosal Treg responses and exacerbates intestinal inflammation. Mechanistically, PGE2-modified microbiota regulates intestinal mononuclear phagocytes and type I interferon signaling. Depletion of mononuclear phagocytes or deficiency of type I interferon receptor diminishes PGE2-dependent Treg inhibition. Together, our findings provide emergent evidence that PGE2-mediated disruption of microbiota-Treg communication fosters intestinal inflammation.

| S-EPMC7880593 | biostudies-literature

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