Similar Datasets
Project description:Specific microbial signals induce the differentiation of a distinct pool of RORγ+ regulatory T (Treg) cells crucial for intestinal homeostasis. We discovered highly analogous populations of microbiota-dependent Treg cells that promoted tissue regeneration at extra-gut sites, notably acutely injured skeletal muscle and fatty liver. Inflammatory meditators elicited by tissue damage combined with MHC-class-II-dependent T cell activation to drive the accumulation of gut-derived RORγ+ Treg cells in injured muscle, wherein they regulated the dynamics and tenor of early inflammation and helped balance the proliferation vs. differentiation of local stem cells. Reining in IL-17A-producing T cells was a major mechanism underlying the rheostatic functions of RORγ+ Treg cells in compromised tissues. Our findings highlight the importance of gut-trained Treg cell emissaries in controlling the response to sterile injury of non-mucosal tissues.
| S-EPMC10101925 | biostudies-literature
Project description:Specific microbial signals induce the differentiation of a distinct pool of RORγ+ regulatory T cells (Tregs) crucial for intestinal homeostasis. We discovered highly analogous populations of microbiota-dependent Tregs that promote tissue regeneration at extra-gut sites, notably acutely injured skeletal muscle and fatty liver. Tissue damage elicited the emigration of RORγ+ Tregs from the gut to compromised tissues, wherein they regulated the dynamics and tenor of early inflammation and helped balance the proliferation versus differentiation of local stem cells. Reining in IL-17A-producing T cells was a major mechanism underlying these rheostatic functions. Our findings highlight the importance of gut-trained Treg emissaries in controlling the response to sterile injury of non-mucosal tissues.
2022-05-01 | GSE196337 | GEO
Project description:Specific microbial signals induce the differentiation of a distinct pool of RORγ+ regulatory T cells (Tregs) crucial for intestinal homeostasis. We discovered highly analogous populations of microbiota-dependent Tregs that promote tissue regeneration at extra-gut sites, notably acutely injured skeletal muscle and fatty liver. Tissue damage elicited the emigration of RORγ+ Tregs from the gut to compromised tissues, wherein they regulated the dynamics and tenor of early inflammation and helped balance the proliferation versus differentiation of local stem cells. Reining in IL-17A-producing T cells was a major mechanism underlying these rheostatic functions. Our findings highlight the importance of gut-trained Treg emissaries in controlling the response to sterile injury of non-mucosal tissues.
2022-05-01 | GSE195966 | GEO
Project description:The gut microbiota promotes distal tissue regeneration via RORγ+ regulatory T cell emissaries
| PRJNA804431 | ENA
Project description:The gut microbiota promotes distal tissue regeneration via RORγ+ regulatory T cell emissaries [scRNA-seq]
| PRJNA804433 | ENA
Project description:The gut microbiota promotes distal tissue regeneration via RORγ+ regulatory T cell emissaries [bulk RNA-seq]
| PRJNA802841 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-10-13 | GSE140887 | GEO
Project description:The metabolic pathways encoded by the human gut microbiome constantly interact with host gene products through numerous bioactive molecules1. Primary bile acids (BAs) are synthesized within hepatocytes and released into the duodenum to facilitate absorption of lipids or fat-soluble vitamins2. Some BAs (approximately 5%) escape into the colon, where gut commensal bacteria convert them into various intestinal BAs2 that are important hormones that regulate host cholesterol metabolism and energy balance via several nuclear receptors and/or G-protein-coupled receptors3,4. These receptors have pivotal roles in shaping host innate immune responses1,5. However, the effect of this host-microorganism biliary network on the adaptive immune system remains poorly characterized. Here we report that both dietary and microbial factors influence the composition of the gut BA pool and modulate an important population of colonic FOXP3+ regulatory T (Treg) cells expressing the transcription factor RORγ. Genetic abolition of BA metabolic pathways in individual gut symbionts significantly decreases this Treg cell population. Restoration of the intestinal BA pool increases colonic RORγ+ Treg cell counts and ameliorates host susceptibility to inflammatory colitis via BA nuclear receptors. Thus, a pan-genomic biliary network interaction between hosts and their bacterial symbionts can control host immunological homeostasis via the resulting metabolites.
| S-EPMC7274525 | biostudies-literature
Project description:Background and aimsCrohn's disease [CD] is associated with complex microbe-host interactions, involving changes in microbial communities, and gut barrier defects, leading to the translocation of microorganisms to surrounding adipose tissue [AT]. We evaluated the presence of beige AT depots in CD and questioned whether succinate and/or bacterial translocation promotes white-to-beige transition in adipocytes.MethodsVisceral [VAT] and subcutaneous [SAT] AT biopsies, serum and plasma were obtained from patients with active [n = 21] or inactive [n = 12] CD, and from healthy controls [n = 15]. Adipose-derived stem cells [ASCs] and AT macrophages [ATMs] were isolated from VAT biopsies.ResultsPlasma succinate levels were significantly higher in patients with active CD than in controls and were intermediate in those with inactive disease. Plasma succinate correlated with the inflammatory marker high-sensitivity C-reactive protein. Expression of the succinate receptor SUCNR1 was higher in VAT, ASCs and ATMs from the active CD group than from the inactive or control groups. Succinate treatment of ASCs elevated the expression of several beige AT markers from controls and from patients with inactive disease, including uncoupling protein-1 [UCP1]. Notably, beige AT markers were prominent in ASCs from patients with active CD. Secretome profiling revealed that ASCs from patients with active disease secrete beige AT-related proteins, and co-culture assays showed that bacteria also trigger the white-to-beige switch of ASCs from patients with CD. Finally, AT depots from patients with CD exhibited a conversion from white to beige AT together with high UCP1 expression, which was corroborated by in situ thermal imaging analysis.ConclusionsSuccinate and bacteria trigger white-to-beige AT transition in CD. Understanding the role of beige AT in CD might aid in the development of therapeutic or diagnostic interventions.
| S-EPMC9624294 | biostudies-literature
Project description:Tissue physiology and responses to injury can be controlled by the cross-talk between all physiological systems including the nervous and immune system. How the microbiota influences this dialogue remains unclear. Here, we show that adaptive responses to the microbiota directly promote sensory neuron regeneration. At homeostasis, commensal-specific Th17 co-localize with sensory neurons within the dermis and display a transcriptional profile associated with tissue and nerve repair. Following injury, commensal-specific Th17 cells promote axon growth and local nerve regeneration. Mechanistically, our data support the idea that IL17-A produced by commensal-specific T cells directly signal sensory neurons via IL17RA, the transcription of which is specifically upregulated in injured neurons. Collectively our work reveals that microbiota-specific T cells can bridge biological systems by directly promoting neuronal repair and identify IL17-A as a major determinant of this fundamental process.
2023-02-07 | GSE196994 | GEO