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11 results on '"Jacquemin, Godefroy"'

3. Leishmania infantum-exploited Nrf2 transcription factor as a virulence process to escape macrophage-driven ferroptosis-like leishmanicidal process

Author

Coste, Agnès, primary, Blot, Clément, additional, Coulson, Kimberley, additional, Salon, Marie, additional, Tertrais, Margot, additional, Planes, Remi, additional, Santoni, Karin, additional, Authier, Hélène, additional, Jacquemin, Godefroy, additional, Rahabi, Mouna, additional, Parny, Mélissa, additional, Raymond-Letron, Isabelle, additional, Meunier, Etienne, additional, and Lefèvre, Lise, additional

Published
2023
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4. PPARγ activation modulates the balance of peritoneal macrophage populations to suppress ovarian tumor growth and tumor-induced immunosuppression

Author

Prat, Mélissa, primary, Coulson, Kimberley, additional, Blot, Clément, additional, Jacquemin, Godefroy, additional, Romano, Mathilde, additional, Renoud, Marie-Laure, additional, AlaEddine, Mohamad, additional, Le Naour, Augustin, additional, Authier, Hélène, additional, Rahabi, Mouna Chirine, additional, Benmoussa, Khaddouj, additional, Salon, Marie, additional, Parny, Mélissa, additional, Delord, Jean-Pierre, additional, Ferron, Gwenaël, additional, Lefèvre, Lise, additional, Couderc, Bettina, additional, and Coste, Agnès, additional

Published
2023
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5. The antitumoral activity of TLR7 ligands is corrupted by the microenvironment of pancreatic tumors

Author

Rouanet, Marie, primary, Hanoun, Naima, additional, Lulka, Hubert, additional, Ferreira, Cindy, additional, Garcin, Pierre, additional, Sramek, Martin, additional, Jacquemin, Godefroy, additional, Coste, Agnès, additional, Pagan, Delphine, additional, Valle, Carine, additional, Sarot, Emeline, additional, Pancaldi, Vera, additional, Lopez, Frédéric, additional, Buscail, Louis, additional, and Cordelier, Pierre, additional

Published
2022
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6. Leishmania infantumexploits the anti-ferroptosis effects of Nrf2 to escape cell death in macrophages

Author

Blot, Clément, Lavernhe, Mathilde, Lugo-Villarino, Geanncarlo, Coulson, Kimberley, Salon, Marie, Tertrais, Margot, Planès, Rémi, Santoni, Karin, Authier, Hélène, Jacquemin, Godefroy, Rahabi, Mouna, Parny, Mélissa, Letron, Isabelle Raymond, Meunier, Etienne, Lefèvre, Lise, and Coste, Agnès

Abstract

Macrophages are major host cells for the protozoan Leishmaniaparasite. Depending on their activation state, they either contribute to the detection and elimination of Leishmaniaspp. or promote parasite resilience. Here, we report that the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) in macrophages plays a pivotal role in the progression of Leishmania infantuminfection by controlling inflammation and redox balance of macrophages. We also highlight the involvement of the NOX2/reactive oxygen species (ROS) axis in early Nrf2 activation and, subsequently, prostaglandin E2 (PGE2)/EP2r signaling in the sustenance of Nrf2 activation upon infection. Moreover, we establish a ferroptosis-like process within macrophages as a cell death program of L. infantumand the protective effect of Nrf2 in macrophages against L. infantumdeath. Altogether, these results identify Nrf2 as a critical factor for the susceptibility of L. infantuminfection, highlighting Nrf2 as a promising pharmacological target for the development of therapeutic approaches for the treatment of visceral leishmaniasis.

Published
2024
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7. Divergent Roles for Macrophage C-type Lectin Receptors, Dectin-1 and Mannose Receptors, in the Intestinal Inflammatory Response

Author

Rahabi, Mouna, Jacquemin, Godefroy, Prat, Mélissa, Meunier, Etienne, Alaeddine, Mohamad, Bertrand, Bénédicte, Lefèvre, Lise, Benmoussa, Khaddouj, Batigne, Philippe, Aubouy, Agnès, Auwerx, Johan, Kirzin, Sylvain, Bonnet, Delphine, Danjoux, Marie, Pipy, Bernard, Alric, Laurent, Authier, Hélène, Coste, Agnès, Pharmacochimie et Biologie pour le Développement (PHARMA-DEV), Institut de Recherche pour le Développement (IRD)-Institut de Chimie de Toulouse (ICT), Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT), Ecole Polytechnique Fédérale de Lausanne (EPFL), Centre Hospitalier Universitaire de Toulouse (CHU Toulouse), Institut de Recherche en Santé Digestive (IRSD ), Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Delegation Regionale a la Recherche Clinique des Hopitaux de Toulouse, France : NCT01990716, Fondation pour la Recherche Medicale, France (FRM) : ECO20170637477, University Hospital of Toulouse, ANR-10-AIRT-0003,BIOASTER,BIOASTER(2010), Institut de Recherche pour le Développement (IRD)-Institut de Chimie de Toulouse (ICT-FR 2599), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut de Recherche pour le Développement (IRD)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, Institut de pharmacologie et de biologie structurale (IPBS), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Infections Parasitaires : Transmission, Physiopathologie et Thérapeutiques (IP-TPT), Service de Santé des Armées-Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU)-Institut de Recherche pour le Développement (IRD), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Institut Suisse de Recherches Expérimentales sur le Cancer Lausanne (EPFL) (ISREC - EPFL), and CHU Toulouse [Toulouse]

Subjects
Adult, Male, Colon, Inflammasomes, Receptors, CCR2, C-type lectin receptor, colitis, [SDV]Life Sciences [q-bio], Interleukin-1beta, IBD, Down-Regulation, Receptors, Cell Surface, macrophage, Leukotriene B4, Young Adult, inflammatory bowel disease, mucosal immmunity, Animals, Antigens, Ly, Humans, Lectins, C-Type, Chemokine CCL2, ComputingMilieux_MISCELLANEOUS, Aged, mannose receptor, Aged, 80 and over, Inflammation, Arachidonate 5-Lipoxygenase, Macrophages, Middle Aged, Inflammatory Bowel Diseases, Intestines, Mice, Inbred C57BL, Mannose-Binding Lectins, innate immune response, Female, Dectin-1, Signal Transduction
Abstract

International audience; Colonic macrophages are considered to be major effectors of inflammatory bowel diseases (IBDs) and the control of gut inflammation through C-type lectin receptors is an emerging concept. We show that during colitis, the loss of dectin-1 on myeloid cells prevents intestinal inflammation, while the lack of mannose receptor (MR) exacerbates it. A marked increase in dectin-1 expression in dextran sulfate sodium (DSS)-exposed MR-deficient mice supports the critical contribution of dectin-1 to colitis outcome. Dectin-1 is crucial for Ly6C(high)CCR2(high) monocyte population enrichment in the blood and their recruitment to inflamed colon as precursors of inflammatory macrophages. Dectin-1 also promotes inflammasome-dependent interleukin-1 beta (IL-1 beta) secretion through leukotriene B4 production. Interestingly, colonic inflammation is associated with a concomitant overexpression of dectin-1/CCL2/LTA4H and downregulation of MR on macrophages from IBD patients. Thus, MR and dectin-1 on macrophages are important mucosal inflammatory regulators that contribute to the intestinal inflammation.

Published
2020

8. Circulating CD14highCD16lowintermediate blood monocytes as a biomarker of ascites immune status and ovarian cancer progression

Author

Prat, Mélissa, primary, Le Naour, Augustin, additional, Coulson, Kimberley, additional, Lemée, Fanny, additional, Leray, Hélène, additional, Jacquemin, Godefroy, additional, Rahabi, Mouna Chirine, additional, Lemaitre, Léa, additional, Authier, Hélène, additional, Ferron, Gwenaël, additional, Barret, Jean-Marc, additional, Martinez, Alejandra, additional, Ayyoub, Maha, additional, Delord, Jean-Pierre, additional, Gladieff, Laurence, additional, Tabah-Fisch, Isabelle, additional, Prost, Jean-François, additional, Couderc, Bettina, additional, and Coste, Agnès, additional

Published
2020
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9. Divergent Roles for Macrophage C-Type Lectin Receptors, Dectin-1 and Mannose Receptors, in Inflammatory Bowel Diseases

Author

Rahabi, Mouna, primary, Jacquemin, Godefroy, additional, Prat, Mélissa, additional, Meunier, Etienne, additional, AlaEddine, Mohamad, additional, Bertrand, Bénédicte, additional, Lefèvre, Lise, additional, Benmoussa, Khaddouj, additional, Batigne, Philippe, additional, Aubouy, Agnès, additional, Auwerx, Johan, additional, Kirzin, Sylvain, additional, Bonnet, Delphine, additional, Danjoux, Marie, additional, Pipy, Bernard, additional, Alric, Laurent, additional, Coste, Agnès, additional, and Authier, Hélène, additional

Published
2019
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10. Circulating CD14 high CD16 low intermediate blood monocytes as a biomarker of ascites immune status and ovarian cancer progression.

Author

Prat M, Le Naour A, Coulson K, Lemée F, Leray H, Jacquemin G, Rahabi MC, Lemaitre L, Authier H, Ferron G, Barret JM, Martinez A, Ayyoub M, Delord JP, Gladieff L, Tabah-Fisch I, Prost JF, Couderc B, and Coste A

Subjects
Disease Progression, Female, Humans, Tumor Microenvironment, Ascites genetics, Biomarkers, Tumor metabolism, Immunotherapy methods, Lipopolysaccharide Receptors metabolism, Monocytes metabolism, Receptors, IgG metabolism
Abstract

Background: Besides the interest of an early detection of ovarian cancer, there is an urgent need for new predictive and prognostic biomarkers of tumor development and cancer treatment. In healthy patients, circulating blood monocytes are typically subdivided into classical (85%), intermediate (5%) and non-classical (10%) populations. Although these circulating monocyte subsets have been suggested as biomarkers in several diseases, few studies have investigate their potential as a predictive signature for tumor immune status,tumor growth and treatment adaptation., Methods: In this study, we used a homogeneous cohort of 28 chemotherapy-naïve patients with ovarian cancer to evaluate monocyte subsets as biomarkers of the ascites immunological status. We evaluated the correlations between circulating monocyte subsets and immune cells and tumor burden in peritoneal ascites. Moreover, to validate the use of circulating monocyte subsets tofollow tumor progression and treatment response, we characterized blood monocytes from ovarian cancer patients included in a phase 1 clinical trial at baseline and following murlentamab treatment., Results: We demonstrate here a robust expansion of the intermediate blood monocytes (IBMs) in ovarian cancer patients. We establish a significant positive correlation between IBM percentage and tumor-associate macrophages with a CCR2 high /CD163 high /CD206 high /CD86 low profile. Moreover, IBM expansion is associated with a decreased effector/regulatory T-cell ratio in ascites and with the presence of soluble immunosuppressive mediators. We also establish that IBM proportion positively correlates with the peritoneum tumor burden. Finally, the study of IBMs in patients with ovarian cancer under immunotherapy during the phase clinical trial supports IBMs to follow the evolution of tumor development and the treatment adaptation., Conclusions: This study, which links IBM level with immunosuppression and tumor burden in peritoneum, identifies IBMs as apotential predictive signature of ascites immune status and as a biomarker ofovarian cancer development and treatment response., Trial Registration Number: EudraCT: 2015-004252-22 NCT02978755., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2020
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11. Divergent Roles for Macrophage C-type Lectin Receptors, Dectin-1 and Mannose Receptors, in the Intestinal Inflammatory Response.

Author

Rahabi M, Jacquemin G, Prat M, Meunier E, AlaEddine M, Bertrand B, Lefèvre L, Benmoussa K, Batigne P, Aubouy A, Auwerx J, Kirzin S, Bonnet D, Danjoux M, Pipy B, Alric L, Authier H, and Coste A

Subjects
Adult, Aged, Aged, 80 and over, Animals, Antigens, Ly metabolism, Arachidonate 5-Lipoxygenase metabolism, Chemokine CCL2 metabolism, Colitis pathology, Colon pathology, Down-Regulation, Female, Humans, Inflammasomes metabolism, Inflammatory Bowel Diseases pathology, Interleukin-1beta metabolism, Leukotriene B4 metabolism, Male, Mannose Receptor, Mice, Inbred C57BL, Middle Aged, Receptors, CCR2 metabolism, Signal Transduction, Young Adult, Inflammation metabolism, Intestines pathology, Lectins, C-Type metabolism, Macrophages metabolism, Mannose-Binding Lectins metabolism, Receptors, Cell Surface metabolism
Abstract

Colonic macrophages are considered to be major effectors of inflammatory bowel diseases (IBDs) and the control of gut inflammation through C-type lectin receptors is an emerging concept. We show that during colitis, the loss of dectin-1 on myeloid cells prevents intestinal inflammation, while the lack of mannose receptor (MR) exacerbates it. A marked increase in dectin-1 expression in dextran sulfate sodium (DSS)-exposed MR-deficient mice supports the critical contribution of dectin-1 to colitis outcome. Dectin-1 is crucial for Ly6C high CCR2 high monocyte population enrichment in the blood and their recruitment to inflamed colon as precursors of inflammatory macrophages. Dectin-1 also promotes inflammasome-dependent interleukin-1β (IL-1β) secretion through leukotriene B4 production. Interestingly, colonic inflammation is associated with a concomitant overexpression of dectin-1/CCL2/LTA4H and downregulation of MR on macrophages from IBD patients. Thus, MR and dectin-1 on macrophages are important mucosal inflammatory regulators that contribute to the intestinal inflammation., Competing Interests: Declaration of Interests The authors declare no competing interests., (Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2020
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