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11 results on '"Patiño-Martínez, Eduardo"'

4. The nuclear receptor Nurr1 is preferentially expressed in human pro-inflammatory macrophages and limits their inflammatory profile

Author

Solís-Barbosa, Miguel A, primary, Santana, Eduardo, additional, Muñoz-Torres, José R, additional, Segovia-Gamboa, Norma C, additional, Patiño-Martínez, Eduardo, additional, Meraz-Ríos, Marco A, additional, Samaniego, Rafael, additional, Sánchez-Mateos, Paloma, additional, and Sánchez-Torres, Carmen, additional

Published
2023
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5. The nuclear receptor Nurr1 is preferentially expressed in human pro-inflammatory macrophages and limits their inflammatory profile.

Author

Solís-Barbosa, Miguel A, Santana, Eduardo, Muñoz-Torres, José R, Segovia-Gamboa, Norma C, Patiño-Martínez, Eduardo, Meraz-Ríos, Marco A, Samaniego, Rafael, Sánchez-Mateos, Paloma, and Sánchez-Torres, Carmen

Subjects
BULLOUS pemphigoid, MACROPHAGE colony-stimulating factor, MACROPHAGES, INFLAMMATORY mediators, REACTIVE oxygen species, NUCLEAR families, GALACTOMANNANS, MACROPHAGE inflammatory proteins
Abstract

Nurr1 is a member of the orphan nuclear receptor family NR4A (nuclear receptor subfamily 4 group A) that modulates inflammation in several cell lineages, both positively and negatively. Macrophages are key regulators of inflammatory responses, yet information about the role of Nurr1 in human macrophages is scarce. Here we examined Nurr1 expression and activity in steady state and activated human macrophages. Pro- and anti-inflammatory macrophages were generated in vitro by culture of blood monocytes with granulocyte/macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF), respectively. Nurr1 expression was predominant in macrophages with the pro-inflammatory phenotype. Nurr1 activation with the agonists 1,1-bis(3ʹ-indolyl)-1-(p -chlorophenyl) methane (C-DIM12) or isoxazolo-pyridinone 7e (IP7e) did not globally modify the polarization status of pro-inflammatory macrophages, but they decreased their production of TNF, IL-1β, IL-6, IL-8, IL-12 p40, CCL2, IFN-β, and reactive oxygen species, with variable potencies. Conversely, Nurr1 deficient macrophages increased the expression of transcripts encoding inflammatory mediators, particularly that of IL6 , IFNB1 , and CCL2. Mechanistically, endogenous Nurr1 interacted with NF-κB p65 in basal conditions and upon lipopolysaccharide (LPS)-mediated activation. C-DIM12 stabilized those complexes in cells exposed to LPS and concurrently decreased NF-κB transcriptional activity and p65 nuclear translocation. Expression of high levels of Nurr1 was associated with a subset of dermal macrophages that display enhanced levels of TNF and lower expression of the anti-inflammatory marker CD163L1 in skin lesions from patients with bullous pemphigoid (BP), a chronic inflammatory autoimmune blistering disorder. These results suggest that Nurr1 expression is linked with the pro-inflammatory phenotype of human macrophages, both in vivo and in vitro , where it may constitute a brake to attenuate the synthesis of inflammatory mediators. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Distinct pathogenic roles for resident and monocyte-derived macrophages in lupus nephritis

Author

Richoz, Nathan, primary, Tuong, Zewen K., additional, Loudon, Kevin W., additional, Patiño-Martínez, Eduardo, additional, Ferdinand, John R., additional, Portet, Anaïs, additional, Bashant, Kathleen R., additional, Thevenon, Emeline, additional, Rucci, Francesca, additional, Hoyler, Thomas, additional, Junt, Tobias, additional, Kaplan, Mariana J., additional, Siegel, Richard M., additional, and Clatworthy, Menna R., additional

Published
2022
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7. 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

8. 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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9. Specific macrophage subsets accumulate in human subcutaneous and omental fat depots during obesity

Author

Girón‐Ulloa, Angélica, primary, González‐Domínguez, Erika, additional, Klimek, Rebeca S, additional, Patiño‐Martínez, Eduardo, additional, Vargas‐Ayala, Germán, additional, Segovia‐Gamboa, Norma C, additional, Campos‐Peña, Victoria, additional, Rodríguez‐Arellano, Martha E, additional, Meraz‐Ríos, Marco A, additional, Campos‐Campos, Salvador F, additional, and Sánchez‐Torres, Carmen, additional

Published
2020
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10. Host-derived lipids from tuberculous pleurisy impair macrophage microbicidal-associated metabolic activity

Author

Franco, José Luis Marín, 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, 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, Layre, Emilie, additional, Hudrisier, Denis, additional, Vérollet, Christel, additional, Neyrolles, Olivier, additional, Sasiain, María Del Carmen, additional, Lugo-Villarino, Geanncarlo, additional, and Balboa, Luciana, additional

Published
2020
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11. 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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