Microbiota-derived pentanoate promotes differentiation of regulatory T cells via enhancing iron uptake in the intestine [FeSO4_treated_Treg]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE195602 | GEO | 2022/01/31
REPOSITORIES: GEO
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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 | GSE195603 | GEO
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
Project description:Analysis of iron-regulated gene expression in Saccharomyces cerevisiae using cDNA microarrays has identified three putative cell wall proteins that are directly regulated by Aft1p, the major iron-dependent transcription factor in yeast. FIT1, FIT2, and FIT3 (for facilitator of iron transport) were more highly expressed in strains grown in low concentrations of iron and in strains in which AFT1-1(up), a constitutively active allele of AFT1, was expressed. Northern blot analysis confirmed that FIT1, FIT2, and FIT3 mRNA transcript levels were increased 60-230-fold in response to iron deprivation in an Aft1p-dependent manner. Fit1p was localized exclusively to the cell wall by indirect immunofluorescence. Deletion of the FIT genes, individually or in combination, resulted in diminished uptake of iron bound to the siderophores ferrioxamine B and ferrichrome, without diminishing the uptake of ferric iron salts, or the siderophores triacetylfusarinine C and enterobactin. FIT-deletion strains exhibited increased expression of Aft1p target genes as measured by a FET3-lacZ reporter gene or by Arn1p Western blotting, indicating that cells respond to the absence of FIT genes by up-regulating systems of iron uptake. Aft1p activation in FIT-deleted strains occurred when either ferrichrome or ferric salts were used as sources of iron during growth, suggesting that the FIT genes enhance uptake of iron from both sources. Enzymatic digestion of the cell wall resulted in the release of significant amounts of iron from cells, and the relative quantity of iron released was reduced in FIT-deletion strains. Fit1p, Fit2p, and Fit3p may function by increasing the amount of iron associated with the cell wall and periplasmic space. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-10-22 | GSE3496 | GEO
Project description:The budding yeast S. cerevisiae responds to depletion of iron in the environment by activating Aft1p, the major iron-dependent transcription factor, and by transcribing systems involved in the uptake of iron. Here we have studied the transcriptional response to iron deprivation, and have identified new Aft1p target genes. We find that other metabolic pathways are regulated by iron: biotin uptake and biosynthesis, nitrogen assimilation, and purine biosynthesis. Two enzymes active in these pathways, biotin synthase and glutamate synthase, require an iron-sulfur cluster for activity. Iron deprivation activates transcription of the biotin importer and simultaneously represses transcription of the entire biotin biosynthetic pathway. Multiple genes involved in nitrogen assimilation and amino acid metabolism are induced by iron deprivation, while glutamate synthase, a key enzyme in nitrogen assimilation, is repressed. A CGG palindrome within the promoter of glutamate synthase confers iron-regulated expression, suggesting control by a transcription factor of the binuclear zinc cluster family. We provide evidence that yeast subjected to iron deprivation undergo a transcriptional remodeling, resulting in a shift from iron-dependent to parallel, but iron-independent, metabolic pathways. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Using regression correlation
2006-02-07 | E-GEOD-4196 | biostudies-arrayexpress
Project description:The budding yeast S. cerevisiae responds to depletion of iron in the environment by activating Aft1p, the major iron-dependent transcription factor, and by transcribing systems involved in the uptake of iron. Here we have studied the transcriptional response to iron deprivation, and have identified new Aft1p target genes. We find that other metabolic pathways are regulated by iron: biotin uptake and biosynthesis, nitrogen assimilation, and purine biosynthesis. Two enzymes active in these pathways, biotin synthase and glutamate synthase, require an iron-sulfur cluster for activity. Iron deprivation activates transcription of the biotin importer and simultaneously represses transcription of the entire biotin biosynthetic pathway. Multiple genes involved in nitrogen assimilation and amino acid metabolism are induced by iron deprivation, while glutamate synthase, a key enzyme in nitrogen assimilation, is repressed. A CGG palindrome within the promoter of glutamate synthase confers iron-regulated expression, suggesting control by a transcription factor of the binuclear zinc cluster family. We provide evidence that yeast subjected to iron deprivation undergo a transcriptional remodeling, resulting in a shift from iron-dependent to parallel, but iron-independent, metabolic pathways. A dose response design type examines the relationship between the size of the administered dose and the extent of the response of the organism(s). Keywords: dose_response_design
2006-02-08 | GSE4196 | GEO
Project description:Effects of different iron replacement methods to gut microbiome of IBD and non IBD patients
| PRJEB48168 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-01-31 | GSE195607 | GEO
Project description:The primary objective of this study is to evaluate the treatment response of Injectafer vs. oral iron to baseline hepcidin levels to determine if any of these select IBD or Gastric Bypass patients may demonstrate to be inappropriate for oral iron therapy.
| 2162662 | ecrin-mdr-crc
Project description:During its life cycle Leishmania undergoes extreme environmental changes, alternating between insect vectors and vertebrate hosts. In mammals the parasites replicate within parasitophorous vacuoles of macrophages, compartments that contain low concentrations of iron. Here we show that stimulation of iron transport, which is induced in Leishmania amazonensis by an iron-poor environment, triggers the differentiation of avirulent promastigotes into virulent amastigotes. Iron depletion from the culture medium triggered expression of the LIT1 ferrous iron transporter, growth arrest, and differentiation of wild type promastigotes into infective amastigotes. In contrast, LIT1 null promastigotes showed continued exponential growth in iron-poor media, followed by massive cell death. Iron depletion from the medium and LIT1 upregulation increased iron superoxide dismutase activity (FeSOD) in wild type, but not in LIT1 null parasites. Notably, the superoxide-generating drug menadione or H2O2 were sufficient to trigger differentiation of wild type promastigotes into fully infective amastigotes. On the other hand, LIT1 null promastigotes accumulated superoxide radical and initiated amastigote differentiation after exposure to H2O2, but not to menadione. Our results reveal a novel role for FeSOD activity and reactive oxygen species (ROS) in orchestrating the differentiation of Leishmania infective stages, in a process regulated by iron availability. Four samples were obtained in total from wild-type L. amazonensis promastigotes grown for 24 hours in culture. Two of these samples derived from medium with iron and two from mediam without iron.These two samples derived from each culture served as biological replicates.
2012-12-15 | E-GEOD-41641 | biostudies-arrayexpress
Project description:During its life cycle Leishmania undergoes extreme environmental changes, alternating between insect vectors and vertebrate hosts. In mammals the parasites replicate within parasitophorous vacuoles of macrophages, compartments that contain low concentrations of iron. Here we show that stimulation of iron transport, which is induced in Leishmania amazonensis by an iron-poor environment, triggers the differentiation of avirulent promastigotes into virulent amastigotes. Iron depletion from the culture medium triggered expression of the LIT1 ferrous iron transporter, growth arrest, and differentiation of wild type promastigotes into infective amastigotes. In contrast, LIT1 null promastigotes showed continued exponential growth in iron-poor media, followed by massive cell death. Iron depletion from the medium and LIT1 upregulation increased iron superoxide dismutase activity (FeSOD) in wild type, but not in LIT1 null parasites. Notably, the superoxide-generating drug menadione or H2O2 were sufficient to trigger differentiation of wild type promastigotes into fully infective amastigotes. On the other hand, LIT1 null promastigotes accumulated superoxide radical and initiated amastigote differentiation after exposure to H2O2, but not to menadione. Our results reveal a novel role for FeSOD activity and reactive oxygen species (ROS) in orchestrating the differentiation of Leishmania infective stages, in a process regulated by iron availability.
2012-12-15 | GSE41641 | GEO