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19 results on '"Métais, Arnaud"'

1. Ezrin, radixin, and moesin are dispensable for macrophage migration and cellular cortex mechanics

Author

Verdys, Perrine, Rey Barroso, Javier, Girel, Adeline, Vermeil, Joseph, Bergert, Martin, Sanchez, Thibaut, Métais, Arnaud, Mangeat, Thomas, Bellard, Elisabeth, Bigot, Claire, Astarie-Dequeker, Catherine, Labrousse, Arnaud, Girard, Jean-Philippe, Maridonneau-Parini, Isabelle, Vérollet, Christel, Lagarrigue, Frédéric, Diz-Muñoz, Alba, Heuvingh, Julien, Piel, Matthieu, du Roure, Olivia, Le Cabec, Véronique, Carréno, Sébastien, and Poincloux, Renaud

Published
2024
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2. Fine-Tuning Levels of Filamins A and B as a Specific Mechanism Sustaining Th2 Lymphocyte Functions

Author

Lutz, Pierre, primary, Maire, Kilian, additional, Ghazali, Samira, additional, Carratala-Lasserre, Manon, additional, Zahm, Margot, additional, Bouisset, Clément, additional, Métais, Arnaud, additional, Combes-Soia, Lucie, additional, Fuente-Vizuete, Lidia de la, additional, Trad, Hussein, additional, Chaubet, Adeline, additional, Savignac, Magali, additional, Gonzalez-de-Peredo, Anne, additional, Subramaniam, Arun, additional, Joffre, Olivier, additional, and Lamsoul, Isabelle, additional

Published
2024
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3. The membrane-actin linkers ezrin, radixin, and moesin are dispensable for macrophage migration and cortex mechanics

Author

Verdys, Perrine, primary, Barroso, Javier Rey, additional, Vermeil, Joseph, additional, Bergert, Martin, additional, Sanchez, Thibaut, additional, Métais, Arnaud, additional, Mangeat, Thomas, additional, Bellard, Elisabeth, additional, Bigot, Claire, additional, Girard, Jean-Philippe, additional, Maridonneau-Parini, Isabelle, additional, Vérollet, Christel, additional, Lagarrigue, Frédéric, additional, Diz-Muñoz, Alba, additional, Heuvingh, Julien, additional, Piel, Matthieu, additional, Roure, Olivia Du, additional, Cabec, Véronique Le, additional, Carréno, Sébastien, additional, and Poincloux, Renaud, additional

Published
2023
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7. Productive HIV-1 infection of tissue macrophages by fusion with infected CD4+ T cells

Author

Mascarau, Rémi, primary, Woottum, Marie, additional, Fromont, Léa, additional, Gence, Rémi, additional, Cantaloube-Ferrieu, Vincent, additional, Vahlas, Zoï, additional, Lévêque, Kevin, additional, Bertrand, Florent, additional, Beunon, Thomas, additional, Métais, Arnaud, additional, El Costa, Hicham, additional, Jabrane-Ferrat, Nabila, additional, Gallois, Yohan, additional, Guibert, Nicolas, additional, Davignon, Jean-Luc, additional, Favre, Gilles, additional, Maridonneau-Parini, Isabelle, additional, Poincloux, Renaud, additional, Lagane, Bernard, additional, Bénichou, Serge, additional, Raynaud-Messina, Brigitte, additional, and Vérollet, Christel, additional

Published
2023
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10. A Pulmonary Lactobacillus murinus Strain Induces Th17 and RORγt + Regulatory T Cells and Reduces Lung Inflammation in Tuberculosis

Author

Bernard-Raichon, Lucie, Colom, André, Monard, Sarah, Namouchi, Amine, Cescato, Margaux, Garnier, Hugo, Leon-Icaza, Stephen, Métais, Arnaud, Dumas, Alexia, Corral, Dan, Ghebrendrias, Natsinet, Guilloton, Pauline, Vérollet, Christel, Hudrisier, Denis, Remot, Aude, Langella, Philippe, Thomas, Muriel, Cougoule, Céline, Neyrolles, Olivier, Lugo-Villarino, Geanncarlo, Marín Franco, José Luis, Genoula, Melanie, Duette, Gabriel, Ferreyra, Malena, Maio, Mariano, Dolotowicz, María Belén, Aparicio-Trejo, Omar Emiliano, Patiño-Martínez, Eduardo, Charton, Alison, Fuentes, Federico, Soldan, Vanessa, Moraña, Eduardo José, Palmero, Domingo, Ostrowski, Matías, Schierloh, Pablo, Sánchez-Torres, Carmen, Hernández-Pando, Rogelio, Pedraza-Chaverri, José, Rombouts, Yoann, Layre, Emilie, Maridonneau-Parini, Isabelle, Sasiain, María del Carmen, Balboa, Luciana, Institut de pharmacologie et de biologie structurale (IPBS), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre for Ecological and Evolutionary Synthesis (CEES), Department of Biosciences [Oslo], Faculty of Mathematics and Natural Sciences [Oslo], University of Oslo (UiO)-University of Oslo (UiO)-Faculty of Mathematics and Natural Sciences [Oslo], University of Oslo (UiO)-University of Oslo (UiO), Université de Toulouse (UT)-Université de Toulouse (UT)-Centre National de la Recherche Scientifique (CNRS), Norwegian University of Life Sciences (NMBU), MICrobiologie de l'ALImentation au Service de la Santé (MICALIS), AgroParisTech-Université Paris-Saclay-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Infectiologie et Santé Publique (UMR ISP), Université de Tours (UT)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), CNRS, Fondation pour la Recherche Medicale (DEQ2016 0334894, FDT201805005210), Fondation Bettencourt Schueller, ANR-15-CE15-0012,MMI-TB,Rôle du microbiome dans la réponse des macrophages à Mycobacterium tuberculosis: un programme de recherche intégrant le microbiote, le métabolisme et l'immunité(2015), ANR-18-CE15-0004,GENDER-TB,Bases immunologiques de la susceptibilité différentielle des genres à la tuberculose(2018), and European Project: 267196,EC:FP7:PEOPLE,FP7-PEOPLE-2010-COFUND,AGREENSKILLS(2012)

Subjects
Tuberculosis, Regulatory T cell, T cell, [SDV]Life Sciences [q-bio], Immunology, Inflammation, Mycobacterium tuberculosis, 03 medical and health sciences, 0302 clinical medicine, Immunity, RAR-related orphan receptor gamma, Immunology and Allergy, Medicine, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, 0303 health sciences, Lung, biology, business.industry, biology.organism_classification, medicine.disease, 3. Good health, medicine.anatomical_structure, medicine.symptom, business, 030215 immunology
Abstract

The lungs harbor multiple resident microbial communities, otherwise known as the microbiota. There is an emerging interest in deciphering whether the pulmonary microbiota modulate local immunity, and whether this knowledge could shed light on mechanisms operating in the response to respiratory pathogens. In this study, we investigate the capacity of a pulmonary Lactobacillus strain to modulate the lung T cell compartment and assess its prophylactic potential upon infection with Mycobacterium tuberculosis, the etiological agent of tuberculosis. In naive mice, we report that a Lactobacillus murinus (Lagilactobacillus murinus) strain (CNCM I-5314) increases the presence of lung Th17 cells and of a regulatory T cell (Treg) subset known as RORγt+ Tregs. In particular, intranasal but not intragastric administration of CNCM I-5314 increases the expansion of these lung leukocytes, suggesting a local rather than systemic effect. Resident Th17 and RORγt+ Tregs display an immunosuppressive phenotype that is accentuated by CNCM I-5314. Despite the well-known ability of M. tuberculosis to modulate lung immunity, the immunomodulatory effect by CNCM I-5314 is dominant, as Th17 and RORγt+ Tregs are still highly increased in the lung at 42-d postinfection. Importantly, CNCM I-5314 administration in M. tuberculosis–infected mice results in reduction of pulmonary inflammation, without increasing M. tuberculosis burden. Collectively, our findings provide evidence for an immunomodulatory capacity of CNCM I-5314 at steady state and in a model of chronic inflammation in which it can display a protective role, suggesting that L. murinus strains found in the lung may shape local T cells in mice and, perhaps, in humans.

Published
2021

11. A Pulmonary Lactobacillus murinus Strain Induces Th17 and RORγt+ Regulatory T Cells and Reduces Lung Inflammation in Tuberculosis

Author

Bernard-Raichon, Lucie, primary, Colom, André, additional, Monard, Sarah C., additional, Namouchi, Amine, additional, Cescato, Margaux, additional, Garnier, Hugo, additional, Leon-Icaza, Stephen A., additional, Métais, Arnaud, additional, Dumas, Alexia, additional, Corral, Dan, additional, Ghebrendrias, Natsinet, additional, Guilloton, Pauline, additional, Vérollet, Christel, additional, Hudrisier, Denis, additional, Remot, Aude, additional, Langella, Philippe, additional, Thomas, Muriel, additional, Cougoule, Céline, additional, Neyrolles, Olivier, additional, and Lugo-Villarino, Geanncarlo, additional

Published
2021
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12. Host-Derived Lipids from Tuberculous Pleurisy Impair Macrophage Microbicidal-Associated Metabolic Activity

Author

Marín Franco, José Luis, primary, Genoula, Melanie, additional, Corral, Dan, additional, Duette, Gabriel, additional, Ferreyra, Malena, additional, Maio, Mariano, additional, Dolotowicz, María Belén, additional, Aparicio-Trejo, Omar Emiliano, additional, Patiño-Martínez, Eduardo, additional, Charton, Alison, additional, Métais, Arnaud, additional, Fuentes, Federico, additional, Soldan, Vanessa, additional, Moraña, Eduardo José, additional, Palmero, Domingo, additional, Ostrowski, Matías, additional, Schierloh, Pablo, additional, Sánchez-Torres, Carmen, additional, Hernández-Pando, Rogelio, additional, Pedraza-Chaverri, José, additional, Rombouts, Yoann, additional, Hudrisier, Denis, additional, Layre, Emilie, additional, Vérollet, Christel, additional, Maridonneau-Parini, Isabelle, additional, Neyrolles, Olivier, additional, Sasiain, María Del Carmen, additional, Lugo-Villarino, Geanncarlo, additional, and Balboa, Luciana, additional

Published
2020
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15. Dissemination of Mycobacterium tuberculosis is associated to a SIGLEC1 null variant that limits antigen exchange via trafficking extracellular vesicles

Author

Marín Franco, José Luis, Genoula, Melanie, Corral, Dan, Duette, Gabriel, Ferreyra, Malena, Maio, Mariano, Dolotowicz, María Belén, Aparicio-Trejo, Omar Emiliano, Patiño-Martínez, Eduardo, Charton, Alison, Métais, Arnaud, Fuentes, Federico, Soldan, Vanessa, Moraña, Eduardo José, Palmero, Domingo, Ostrowski, Matías, Schierloh, Pablo, Sánchez-Torres, Carmen, Hernández-Pando, Rogelio, Pedraza-Chaverri, José, Rombouts, Yoann, Hudrisier, Denis, Layre, Emilie, Vérollet, Christel, Maridonneau-Parini, Isabelle, Neyrolles, Olivier, Sasiain, María del Carmen, Lugo-Villarino, Geanncarlo, Balboa, Luciana, Benet, Susana, Gálvez, Cristina, Drobniewski, Francis, Kontsevaya, Irina, Arias, Lilibeth, Monguió‐Tortajada, Marta, Erkizia, Itziar, Urrea, Victor, Ong, Ruo‐Yan, Luquin, Marina, Dupont, Maeva, Chojnacki, Jakub, Dalmau, Judith, Cardona, Paula, Lugo‐Villarino, Geanncarlo, Julián, Esther, Furrer, Hansjakob, Günthard, Huldrych, Crocker, Paul, Tapia, Gustavo, Borràs, Francesc, Fellay, Jacques, McLaren, Paul, Telenti, Amalio, Cardona, Pere‐Joan, Clotet, Bonaventura, Vilaplana, Cristina, Martinez‐Picado, Javier, Izquierdo‐Useros, Nuria, Institut de pharmacologie et de biologie structurale (IPBS), Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Wellcome Trust, Imperial College Trust, and Commission of the European Communities

Subjects
0301 basic medicine, Histology, [SDV]Life Sciences [q-bio], Antigen presentation, 610 Medicine & health, hiv-1, Biology, 0601 Biochemistry and Cell Biology, Microbiology, Mycobacterium tuberculosis, 03 medical and health sciences, 0302 clinical medicine, Antigen, Receptor, Gene, ComputingMilieux_MISCELLANEOUS, Extracellular vesicles, HIV‐1, Mtb, Siglec‐1, Science & Technology, Siglec-1, QH573-671, Extracellular vesicle, Cell Biology, respiratory system, biology.organism_classification, Null allele, siglec-1, 3. Good health, 030104 developmental biology, 030220 oncology & carcinogenesis, Knockout mouse, HIV-1, Cytology, Life Sciences & Biomedicine
Abstract

The identification of individuals with null alleles enables studying how the loss of gene function affects infection. We previously described a non‐functional variant in SIGLEC1, which encodes the myeloid‐cell receptor Siglec‐1/CD169 implicated in HIV‐1 cell‐to‐cell transmission. Here we report a significant association between the SIGLEC1 null variant and extrapulmonary dissemination of Mycobacterium tuberculosis (Mtb) in two clinical cohorts comprising 6,256 individuals. Local spread of bacteria within the lung is apparent in Mtb‐infected Siglec‐1 knockout mice which, despite having similar bacterial load, developed more extensive lesions compared to wild type mice. We find that Siglec‐1 is necessary to induce antigen presentation through extracellular vesicle uptake. We postulate that lack of Siglec‐1 delays the onset of protective immunity against Mtb by limiting antigen exchange via extracellular vesicles, allowing for an early local spread of mycobacteria that increases the risk for extrapulmonary dissemination.

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16. Productive HIV-1 infection of tissue macrophages by fusion with infected CD4+ T cells.

Author

Mascarau, Rémi, Woottum, Marie, Fromont, Léa, Gence, Rémi, Cantaloube-Ferrieu, Vincent, Vahlas, Zoï, Lévêque, Kevin, Bertrand, Florent, Beunon, Thomas, Métais, Arnaud, El Costa, Hicham, Jabrane-Ferrat, Nabila, Gallois, Yohan, Guibert, Nicolas, Davignon, Jean-Luc, Favre, Gilles, Maridonneau-Parini, Isabelle, Poincloux, Renaud, Lagane, Bernard, and Bénichou, Serge

Subjects
*T cells, *MACROPHAGES, *CELL fusion, *HIV, *TONSILS, *INFECTION, *ACTOMYOSIN
Abstract

Macrophages are essential for HIV-1 pathogenesis and represent major viral reservoirs. Therefore, it is critical to understand macrophage infection, especially in tissue macrophages, which are widely infected in vivo, but poorly permissive to cell-free infection. Although cell-to-cell transmission of HIV-1 is a determinant mode of macrophage infection in vivo, how HIV-1 transfers toward macrophages remains elusive. Here, we demonstrate that fusion of infected CD4+ T lymphocytes with human macrophages leads to their efficient and productive infection. Importantly, several tissue macrophage populations undergo this heterotypic cell fusion, including synovial, placental, lung alveolar, and tonsil macrophages. We also find that this mode of infection is modulated by the macrophage polarization state. This fusion process engages a specific short-lived adhesion structure and is controlled by the CD81 tetraspanin, which activates RhoA/ROCK-dependent actomyosin contractility in macrophages. Our study provides important insights into the mechanisms underlying infection of tissue-resident macrophages, and establishment of persistent cellular reservoirs in patients. [ABSTRACT FROM AUTHOR]

Published
2023
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18. Moesin controls cell-cell fusion and osteoclast function.

Author

Dufrancais O, Verdys P, Plozza M, Métais A, Juzans M, Sanchez T, Bergert M, Halper J, Panebianco CJ, Mascarau R, Gence R, Arnaud G, Neji MB, Maridonneau-Parini I, Cabec VL, Boerckel JD, Pavlos NJ, Diz-Muñoz A, Lagarrigue F, Blin-Wakkach C, Carréno S, Poincloux R, Burkhardt JK, Raynaud-Messina B, and Vérollet C

Abstract

Cell-cell fusion is an evolutionarily conserved process that is essential for many functions, including fertilisation and the formation of placenta, muscle and osteoclasts, multinucleated cells that are unique in their ability to resorb bone. The mechanisms of osteoclast multinucleation involve dynamic interactions between the actin cytoskeleton and the plasma membrane that are still poorly characterized. Here, we found that moesin, a cytoskeletal linker protein member of the Ezrin/Radixin/Moesin (ERM) protein family, is activated during osteoclast maturation and plays an instrumental role in both osteoclast fusion and function. In mouse and human osteoclast precursors, moesin inhibition favors their ability to fuse into multinucleated osteoclasts. Accordingly, we demonstrated that moesin depletion decreases membrane-to-cortex attachment and enhances the formation of tunneling nanotubes (TNTs), F-actin-based intercellular bridges that we reveal here to trigger cell-cell fusion. Moesin also controls HIV-1- and inflammation-induced cell fusion. In addition, moesin regulates the formation of the sealing zone, the adhesive structure determining osteoclast bone resorption area, and thus controls bone degradation, via a β3-integrin/RhoA/SLK pathway. Supporting our results, moesin - deficient mice present a reduced density of trabecular bones and increased osteoclast abundance and activity. These findings provide a better understanding of the regulation of cell-cell fusion and osteoclast biology, opening new opportunities to specifically target osteoclast activity in bone disease therapy.

Published
2024
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19. A Pulmonary Lactobacillus murinus Strain Induces Th17 and RORγt + Regulatory T Cells and Reduces Lung Inflammation in Tuberculosis.

Author

Bernard-Raichon L, Colom A, Monard SC, Namouchi A, Cescato M, Garnier H, Leon-Icaza SA, Métais A, Dumas A, Corral D, Ghebrendrias N, Guilloton P, Vérollet C, Hudrisier D, Remot A, Langella P, Thomas M, Cougoule C, Neyrolles O, and Lugo-Villarino G

Subjects
Animals, Cells, Cultured, Disease Models, Animal, Humans, Lung microbiology, Lymphocyte Activation, Mice, Mice, Inbred C57BL, Pneumonia, Lactobacillus physiology, Lung immunology, Mycobacterium tuberculosis physiology, Nuclear Receptor Subfamily 1, Group F, Member 3 metabolism, T-Lymphocytes, Regulatory immunology, Th17 Cells immunology, Tuberculosis, Pulmonary immunology
Abstract

The lungs harbor multiple resident microbial communities, otherwise known as the microbiota. There is an emerging interest in deciphering whether the pulmonary microbiota modulate local immunity, and whether this knowledge could shed light on mechanisms operating in the response to respiratory pathogens. In this study, we investigate the capacity of a pulmonary Lactobacillus strain to modulate the lung T cell compartment and assess its prophylactic potential upon infection with Mycobacterium tuberculosis , the etiological agent of tuberculosis. In naive mice, we report that a Lactobacillus murinus ( Lagilactobacillus murinus ) strain (CNCM I-5314) increases the presence of lung Th17 cells and of a regulatory T cell (Treg) subset known as RORγt + Tregs. In particular, intranasal but not intragastric administration of CNCM I-5314 increases the expansion of these lung leukocytes, suggesting a local rather than systemic effect. Resident Th17 and RORγt + Tregs display an immunosuppressive phenotype that is accentuated by CNCM I-5314. Despite the well-known ability of M. tuberculosis to modulate lung immunity, the immunomodulatory effect by CNCM I-5314 is dominant, as Th17 and RORγt + Tregs are still highly increased in the lung at 42-d postinfection. Importantly, CNCM I-5314 administration in M. tuberculosis -infected mice results in reduction of pulmonary inflammation, without increasing M. tuberculosis burden. Collectively, our findings provide evidence for an immunomodulatory capacity of CNCM I-5314 at steady state and in a model of chronic inflammation in which it can display a protective role, suggesting that L. murinus strains found in the lung may shape local T cells in mice and, perhaps, in humans., (Copyright © 2021 by The American Association of Immunologists, Inc.)

Published
2021
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