Search

Your search keyword '"Anne Foussier"' showing total 2 results
Start Over Author "Anne Foussier"
2 results on '"Anne Foussier"'

1. Microbial metabolites control the thymic development of mucosal-associated invariant T cells

Author

Manal Sarkis, Jules Gilet, Kristina Niort, François Legoux, Yara El Morr, Olivier Lantz, Emanuele Procopio, Aurélie Balvay, Ahmed El Marjou, Aurélie Darbois, Frédéric Schmidt, Anne Foussier, Déborah Bellet, Celine Daviaud, Marion Salou, Sylvie Rabot, Bernhard Ryffel, Recherches en cancérologie, Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM), Immunité et cancer (U932), Institut Curie-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Transplantation et Immunologie (U1064 Inserm - CRTI), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Immunologie et Neurogénétique Expérimentales et Moléculaires (INEM), Université d'Orléans (UO)-Centre National de la Recherche Scientifique (CNRS), MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Chimie biologique des membranes et ciblage thérapeutique (CBMCT - UMR 3666 / U1143), Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Curie [Paris]-Centre National de la Recherche Scientifique (CNRS), Université Paris Descartes - Paris 5 (UPD5)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre National de la Recherche Scientifique (CNRS)-Université d'Orléans (UO), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie du CNRS (INC), and Université Paris Descartes - Paris 5 (UPD5)-Institut Curie-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV]Life Sciences [q-bio], Receptors, Antigen, T-Cell, Thymus Gland, Mucosal associated invariant T cell, Major histocompatibility complex, medicine.disease_cause, Mucosal-Associated Invariant T Cells, Minor Histocompatibility Antigens, Mice, 03 medical and health sciences, 0302 clinical medicine, Immune system, Antigen, Escherichia coli, medicine, [CHIM]Chemical Sciences, Animals, Germ-Free Life, Symbiosis, Uracil, Receptor, Lung, ComputingMilieux_MISCELLANEOUS, Ribitol, 030304 developmental biology, Mice, Knockout, Orphan receptor, 0303 health sciences, Mucous Membrane, Multidisciplinary, biology, Escherichia coli Proteins, Histocompatibility Antigens Class I, biology.organism_classification, Gastrointestinal Microbiome, Specific Pathogen-Free Organisms, Cell biology, Mice, Inbred C57BL, Nucleotide Deaminases, biology.protein, Spleen, Bacteria, Sugar Alcohol Dehydrogenases, 030215 immunology
Abstract

Commensals rule the MAITrix Mucosal-associated invariant T (MAIT) cells play an important role in mucosal homeostasis. MAIT cells recognize microbial small molecules presented by the major histocompatibility complex class Ib molecule MR1. MAIT cells are absent in germ-free mice, and the mechanisms by which microbiota control MAIT cell development are unknown (see the Perspective by Oh and Unutmaz). Legoux et al. show that, in mice, development of MAIT cells within the thymus is governed by the bacterial product 5-(2-oxopropylideneamino)-6- d -ribitylaminouracil, which rapidly traffics from the mucosa to the thymus, where it is captured by MR1 and presented to developing MAIT cells. Constantinides et al. report that MAIT cell induction only occurs during a limited, early-life window and requires exposure to defined microbes that produce riboflavin derivatives. Continual interactions between MAIT cells and commensals in the skin modulates tissue repair functions. Together, these papers highlight how the microbiota can direct immune cell development and subsequent function at mucosal sites by secreting compounds that act like self-antigens. Science , this issue p. 494 , p. eaax6624 ; see also p. 419

Published
2019
Full Text
View/download PDF

2. The Mouse Microbiome Is Required for Sex-Specific Diurnal Rhythms of Gene Expression and Metabolism

Author

Aline Charpagne, Francis Foata, Jake Yeung, Benjamin D. Weger, Felix Naef, Bertrand Betrisey, Eva Martin, Frédéric Gachon, Aurélie Balvay, Sonia Jimenez, Cédric Gobet, Bernard Berger, Chieh Jason Chou, Anne Foussier, Brigitte Boizet-Bonhoure, Nestlé Institute of Health Sciences SA [Lausanne, Switzerland], Department of Diabetes and Circadian Rhythms, Nestlé Institute of Health Sciences, 1015 Lausanne, Switzerland., Ecole Polytechnique Fédérale de Lausanne (EPFL), Institute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, 1015 Lausanne, Switzerland., Department of Diabetes and Circadian Rhythms, Nestlé Institute of Health Sciences, 1015 Lausanne, Switzerland, Cellular Metabolism, Department of Cell Biology, Nestlé Institute of Health Sciences, Nestlé Research, 1015 Lausanne, Switzerland., Nestle Res Ctr, Nestec Ltd, Host-Microbe Interaction, Department of Gastro-Intestinal Health, MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Genomics, Department of Multi-Omics, Nestlé Institute of Health Sciences, Nestlé Research, 1015 Lausanne, Switzerland, Institut de génétique humaine (IGH), Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Nestlé Research Center, Nestle Reasearch Center, Institute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, 1015 Lausanne, Switzerland, Swiss National Science Foundation [310030_173079], Natural Sciences and Engineering Research Council of Canada Postgraduate Studies Doctoral Scholarship, European Project: 260988,EC:FP7:ERC,ERC-2010-StG_20091118,CIRCATRANS(2011), Nestlé Research Center | Centre de recherche Nestlé [Lausanne], Nestlé S.A., and School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, 1015 Lausanne, Switzerland

Subjects
0301 basic medicine, Male, Physiology, [SDV]Life Sciences [q-bio], Circadian clock, nuclear receptors, Gene Expression, White adipose tissue, Transcriptome, Mice, 0302 clinical medicine, circadian clock, reproductive function, Sex Characteristics, sexual maturation, Growth hormone secretion, symbiosis, Cell biology, Circadian Rhythm, Intestines, germ-free, ghrelin, Female, diet-induced obesity, Adipose Tissue, White, Feminization (biology), Bcl6, Biology, liver, Article, 03 medical and health sciences, Circadian Clocks, Metabolome, microbiota, Animals, Humans, Microbiome, Molecular Biology, [SDV.GEN]Life Sciences [q-bio]/Genetics, gut microbiota, aryl-hydrocarbon receptor, growth-hormone-secretion, Cell Biology, signaling pathways, Gastrointestinal Microbiome, Mice, Inbred C57BL, Sexual dimorphism, 030104 developmental biology, cyp1a1 expression, sexual dimorphism, growth hormone, 030217 neurology & neurosurgery
Abstract

Summary The circadian clock and associated feeding rhythms have a profound impact on metabolism and the gut microbiome. To what extent microbiota reciprocally affect daily rhythms of physiology in the host remains elusive. Here, we analyzed transcriptome and metabolome profiles of male and female germ-free mice. While mRNA expression of circadian clock genes revealed subtle changes in liver, intestine, and white adipose tissue, germ-free mice showed considerably altered expression of genes associated with rhythmic physiology. Strikingly, the absence of the microbiome attenuated liver sexual dimorphism and sex-specific rhythmicity. The resulting feminization of male and masculinization of female germ-free animals is likely caused by altered sexual development and growth hormone secretion, associated with differential activation of xenobiotic receptors. This defines a novel mechanism by which the microbiome regulates host metabolism., Graphical Abstract, Highlights • The microbiome is required for sexual dimorphism in gene expression and metabolism • Most already-described changes in GF mice are hallmarks of a feminized metabolism • Altered sexual maturation and GH secretion cause the damping of sexual dimorphism • Microbiota-derived metabolites and ghrelin likely drive these alterations, Physiology is dynamic over the day and different between sexes. Weger et al. show that the microbiome play a key role in sustaining these sex differences in gene expression and metabolism by ensuring proper sexual maturation and growth hormone secretion. Microbiota-derived metabolites and ghrelin likely drive these sexually dimorphic dynamics.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results