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Start Over Author "Barbara Misme-Aucouturier" Topic immune tolerance
4 results on '"Barbara Misme-Aucouturier"'

1. Prebiotic Supplementation During Pregnancy Modifies the Gut Microbiota and Increases Metabolites in Amniotic Fluid, Driving a Tolerogenic Environment In Utero

Author

Carole Brosseau, Amandine Selle, Angeline Duval, Barbara Misme-Aucouturier, Melanie Chesneau, Sophie Brouard, Claire Cherbuy, Véronique Cariou, Gregory Bouchaud, Kyle T. Mincham, Deborah H. Strickland, Sebastien Barbarot, and Marie Bodinier

Subjects
prebiotic, pregnancy, gut microbiota, immune tolerance, feto-maternal tissues, immune imprinting, Immunologic diseases. Allergy, RC581-607
Abstract

The gut microbiota is influenced by environmental factors such as food. Maternal diet during pregnancy modifies the gut microbiota composition and function, leading to the production of specific compounds that are transferred to the fetus and enhance the ontogeny and maturation of the immune system. Prebiotics are fermented by gut bacteria, leading to the release of short-chain fatty acids that can specifically interact with the immune system, inducing a switch toward tolerogenic populations and therefore conferring health benefits. In this study, pregnant BALB/cJRj mice were fed either a control diet or a diet enriched in prebiotics (Galacto-oligosaccharides/Inulin). We hypothesized that galacto-oligosaccharides/inulin supplementation during gestation could modify the maternal microbiota, favoring healthy immune imprinting in the fetus. Galacto-oligosaccharides/inulin supplementation during gestation increases the abundance of Bacteroidetes and decreases that of Firmicutes in the gut microbiota, leading to increased production of fecal acetate, which was found for the first time in amniotic fluid. Prebiotic supplementation increased the abundance of regulatory B and T cells in gestational tissues and in the fetus. Interestingly, these regulatory cells remained later in life. In conclusion, prebiotic supplementation during pregnancy leads to the transmission of specific microbial and immune factors from mother to child, allowing the establishment of tolerogenic immune imprinting in the fetus that may be beneficial for infant health outcomes.

Published
2021
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2. Engineering a safe monoclonal anti‐human IL‐2 that is effective in a murine model of food allergy and asthma

Author

Marie-Aude Cheminant, Marie Wauters, Grégory Bouchaud, Marion De Carvalho, Barbara Misme-Aucouturier, Antoine Magnan, Olivier Tranquet, Martin Klein, unité de recherche de l'institut du thorax UMR1087 UMR6291 (ITX), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Unité de recherche sur les Biopolymères, Interactions Assemblages (BIA), Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Antwerp University Hospital [Edegem] (UZA), Fondation du Souffle, Fond de Dotation de Recherche en Santé Respiratoire, INRAE Transfert, 'Institut de Recherche en Sante Respiratoire' IRSR., and ANR-16-IDEX-0007,NExT (I-SITE),NExT (I-SITE)(2016)

Subjects
Allergy, Immunology, Immunoglobulin E, T-Lymphocytes, Regulatory, [SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract, Immune tolerance, Mice, 03 medical and health sciences, 0302 clinical medicine, Food allergy, antibody, [SDV.IDA]Life Sciences [q-bio]/Food engineering, medicine, Animals, Humans, Immunology and Allergy, T lymphocytes, Lymphocytes, dendritic cells, [SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology, 030304 developmental biology, 0303 health sciences, biology, business.industry, IL-2, Innate lymphoid cell, asthma, medicine.disease, Acquired immune system, allergy, Immunity, Innate, 3. Good health, Disease Models, Animal, Monoclonal, biology.protein, Interleukin-2, [SDV.IMM]Life Sciences [q-bio]/Immunology, Antibody, business, Food Hypersensitivity, 030215 immunology
Abstract

International audience; Background Regulatory T cells (Tregs) are known to protect against allergies. Moreover, the decrease in the frequency and efficiency of Tregs amplifies allergic symptoms. Aim This study investigated whether expanding Tregs in vivo with an IL-2/IL-2 antibody complex could be safe, well tolerated and efficient in a therapeutic setting in allergies. Methods We produced an anti-IL-2 antibody (1C6) and demonstrated that when it is complexed to human IL-2, it increases IL-2 efficiency to induce Tregs in vivo without any detectable side effects. Furthermore, the IL-2/1C6 complex induces an increase in Helios expression by Tregs, suggesting that it not only elevated Treg numbers but also boosted their functions. Using mouse models of house-dust-mite-induced airway inflammation and wheat-gliadin-induced food allergies, we investigated the therapeutic potential of the IL-2/1C6 complex in allergies. Results IL-2/1C6 treatment significantly reduced allergic symptoms, specific IgE production, the adaptive immune response and tissue damage. Interestingly, IL-2/1C6 treatment modulated innate lymphoid cells by increasing ILC2s in asthma and decreasing ILC3s in food allergies. Conclusion In conclusion,complexed IL-2/anti-IL-2 may restore Treg numbers and function in respiratory and food allergies, thereby improving allergic markers and symptoms. Our IL-2/anti-IL-2 complex offers new hope for reestablishing immune tolerance in patients with allergies.

Published
2021
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3. Alveolar macrophages are epigenetically altered after inflammation, leading to long-term lung immunoparalysis

Author

Mickael Vourc'h, Marion Davieau, Jose A Villadangos, Antoine Roquilly, Hamish E G McWilliam, Vanessa Gauttier, Abderrahmane Sadek, Raphaël Cinotti, Alexis Broquet, Cédric Jacqueline, Cynthia Fourgeux, Alice Molle, Frédéric Altare, Nadege Marec, Karim Asehnoune, Jeremie Poschmann, Paul Rooze, Barbara Misme-Aucouturier, Tanguy Chaumette, Le Bihan, Sylvie, Thérapeutiques cliniques et expérimentales des infections (EA 3826) (EA 3826), Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), Université de Nantes (UN)-Université de Nantes (UN), Anesthésie Réanimation chirurgicale [CHU Nantes], Centre hospitalier universitaire de Nantes (CHU Nantes)-Hôpital Guillaume-et-René-Laennec [Saint-Herblain], University of Melbourne, 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), Institut de transplantation urologie-néphrologie (ITUN), Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes), Université Moulay Ismail (UMI), Plateforme CYTOCELL Nantes (CRCINA-CYTOCELL), Centre de Recherche en Cancérologie et Immunologie Nantes-Angers (CRCINA), Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Université d'Angers (UA)-Université de Nantes (UN)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre hospitalier universitaire de Nantes (CHU Nantes), Host-Pathogen Interactions in the Regulation of Immune Responses (CRCINA-ÉQUIPE 5), Dendritic cells and immunoregulation in transplantation and immunopathology (Team 1 - U1064 Inserm - CRTI), Université de Nantes (UN)-Université de Nantes (UN)-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 hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Nantes - UFR de Médecine et des Techniques Médicales (UFR MEDECINE), and Université de Nantes (UN)-Université de Nantes (UN)-Centre hospitalier universitaire de Nantes (CHU Nantes)-Centre National de la Recherche Scientifique (CNRS)-Université d'Angers (UA)

Subjects
0301 basic medicine, Phagocytosis, [SDV]Life Sciences [q-bio], Immunology, Inflammation, Systemic inflammation, Immune tolerance, Sepsis, 03 medical and health sciences, 0302 clinical medicine, medicine, Immunology and Allergy, Lung, biology, business.industry, medicine.disease, 3. Good health, [SDV] Life Sciences [q-bio], Pneumonia, 030104 developmental biology, medicine.anatomical_structure, biology.protein, medicine.symptom, Antibody, business, 030215 immunology
Abstract

International audience; Sepsis and trauma cause inflammation and elevated susceptibility to hospital-acquired pneumonia. As phagocytosis by macrophages plays a critical role in the control of bacteria, we investigated the phagocytic activity of macrophages after resolution of inflammation. After resolution of primary pneumonia, murine alveolar macrophages (AMs) exhibited poor phagocytic capacity for several weeks. These paralyzed AMs developed from resident AMs that underwent an epigenetic program of tolerogenic training. Such adaptation was not induced by direct encounter of the pathogen but by secondary immunosuppressive signals established locally upon resolution of primary infection. Signal-regulatory protein α (SIRPα) played a critical role in the establishment of the microenvironment that induced tolerogenic training. In humans with systemic inflammation, AMs and also circulating monocytes still displayed alterations consistent with reprogramming six months after resolution of inflammation. Antibody blockade of SIRPα restored phagocytosis in monocytes of critically ill patients in vitro, which suggests a potential strategy to prevent hospital-acquired pneumonia.

Published
2020
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4. Alveolar macrophages are epigenetically altered after inflammation, leading to long-term lung immunoparalysis

Author

Antoine, Roquilly, Cedric, Jacqueline, Marion, Davieau, Alice, Mollé, Abderrahmane, Sadek, Cynthia, Fourgeux, Paul, Rooze, Alexis, Broquet, Barbara, Misme-Aucouturier, Tanguy, Chaumette, Mickael, Vourc'h, Raphael, Cinotti, Nadege, Marec, Vanessa, Gauttier, Hamish E G, McWilliam, Frederic, Altare, Jeremie, Poschmann, Jose A, Villadangos, and Karim, Asehnoune

Subjects
Inflammation, Macrophages, Pneumonia, Cellular Reprogramming, Monocytes, Epigenesis, Genetic, Immunophenotyping, Mice, Phagocytosis, T-Lymphocyte Subsets, Macrophages, Alveolar, Immune Tolerance, Animals, Cytokines, Humans, Inflammation Mediators, Lung, Biomarkers
Abstract

Sepsis and trauma cause inflammation and elevated susceptibility to hospital-acquired pneumonia. As phagocytosis by macrophages plays a critical role in the control of bacteria, we investigated the phagocytic activity of macrophages after resolution of inflammation. After resolution of primary pneumonia, murine alveolar macrophages (AMs) exhibited poor phagocytic capacity for several weeks. These paralyzed AMs developed from resident AMs that underwent an epigenetic program of tolerogenic training. Such adaptation was not induced by direct encounter of the pathogen but by secondary immunosuppressive signals established locally upon resolution of primary infection. Signal-regulatory protein α (SIRPα) played a critical role in the establishment of the microenvironment that induced tolerogenic training. In humans with systemic inflammation, AMs and also circulating monocytes still displayed alterations consistent with reprogramming six months after resolution of inflammation. Antibody blockade of SIRPα restored phagocytosis in monocytes of critically ill patients in vitro, which suggests a potential strategy to prevent hospital-acquired pneumonia.

Published
2019

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