9 results on '"Cantoni, Eleonora"'
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2. Myelomonocytic cells in giant cell arteritis activate trained immunity programs sustaining inflammation and cytokine production
- Author
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Cantoni, E, Merelli, I, Stefanoni, D, Tomelleri, A, Campochiaro, C, Giordano, V, Panigada, M, Baldissera, E, Merlo Pich, L, Natoli, V, Ziogas, A, Domínguez-Andrés, J, De Luca, G, Mazza, D, Zambrano, S, Gnani, D, Ferrarini, M, Ferrero, E, Agresti, A, Vergani, B, Leone, B, Cenci, S, Ravelli, A, Matucci-Cerinic, M, D'Alessandro, A, Joosten, L, Dagna, L, Netea, M, Molteni, R, Cavalli, G, Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Merlo Pich, Laura, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, De Luca, Giacomo, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, Vergani, Barbara, Leone, Biagio Eugenio, Cenci, Simone, Ravelli, Angelo, Matucci-Cerinic, Marco, D'Alessandro, Angelo, Joosten, Leo A B, Dagna, Lorenzo, Netea, Mihai G, Molteni, Raffaella, Cavalli, Giulio, Cantoni, E, Merelli, I, Stefanoni, D, Tomelleri, A, Campochiaro, C, Giordano, V, Panigada, M, Baldissera, E, Merlo Pich, L, Natoli, V, Ziogas, A, Domínguez-Andrés, J, De Luca, G, Mazza, D, Zambrano, S, Gnani, D, Ferrarini, M, Ferrero, E, Agresti, A, Vergani, B, Leone, B, Cenci, S, Ravelli, A, Matucci-Cerinic, M, D'Alessandro, A, Joosten, L, Dagna, L, Netea, M, Molteni, R, Cavalli, G, Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Merlo Pich, Laura, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, De Luca, Giacomo, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, Vergani, Barbara, Leone, Biagio Eugenio, Cenci, Simone, Ravelli, Angelo, Matucci-Cerinic, Marco, D'Alessandro, Angelo, Joosten, Leo A B, Dagna, Lorenzo, Netea, Mihai G, Molteni, Raffaella, and Cavalli, Giulio
- Abstract
Objective: Trained immunity (TI) is a de facto memory program of innate immune cells, characterized by immunometabolic and epigenetic changes sustaining enhanced production of cytokines. TI evolved as a protective mechanism against infections; however, inappropriate activation can cause detrimental inflammation and might be implicated in the pathogenesis of chronic inflammatory diseases. In this study, we investigated the role of TI in the pathogenesis of giant cell arteritis (GCA), a large-vessel vasculitis characterized by aberrant macrophage activation and excess cytokine production. Methods: Monocytes from GCA patients and from age- and sex-matched healthy donors were subjected to polyfunctional studies, including cytokine production assays at baseline and following stimulation, intracellular metabolomics, chromatin immunoprecipitation-qPCR, and combined ATAC/RNA sequencing. Immunometabolic activation (i.e. glycolysis) was assessed in inflamed vessels of GCA patients with FDG-PET and immunohistochemistry (IHC), and the role of this pathway in sustaining cytokine production was confirmed with selective pharmacologic inhibition in GCA monocytes. Results: GCA monocytes exhibited hallmark molecular features of TI. Specifically, these included enhanced IL-6 production upon stimulation, typical immunometabolic changes (e.g. increased glycolysis and glutaminolysis) and epigenetic changes promoting enhanced transcription of genes governing pro-inflammatory activation. Immunometabolic changes of TI (i.e. glycolysis) were a feature of myelomonocytic cells in GCA lesions and were required for enhanced cytokine production. Conclusions: Myelomonocytic cells in GCA activate TI programs sustaining enhanced inflammatory activation with excess cytokine production.
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- 2023
3. Myelomonocytic cells in giant cell arteritis activate trained immunity programs sustaining inflammation and cytokine production.
- Author
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Cantoni, Eleonora, Merelli, Ivan, Stefanoni, Davide, Tomelleri, Alessandro, Campochiaro, Corrado, Giordano, Vito, Panigada, Maddalena, Baldissera, Elena M, Pich, Laura Merlo, Natoli, Valentina, Ziogas, Athanasios, Domínguez-Andrés, Jorge, Luca, Giacomo De, Mazza, Davide, Zambrano, Samuel, Gnani, Daniela, Ferrarini, Marina, Ferrero, Elisabetta, Agresti, Alessandra, and Vergani, Barbara
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CYTOKINES , *NATURAL immunity , *SEQUENCE analysis , *INFLAMMATION , *CHRONIC diseases , *IMMUNOHISTOCHEMISTRY , *METABOLOMICS , *GIANT cell arteritis , *GENE expression , *GENES , *RESEARCH funding , *MONOCYTES , *VASCULITIS - Abstract
Objective Trained immunity (TI) is a de facto memory program of innate immune cells, characterized by immunometabolic and epigenetic changes sustaining enhanced production of cytokines. TI evolved as a protective mechanism against infections; however, inappropriate activation can cause detrimental inflammation and might be implicated in the pathogenesis of chronic inflammatory diseases. In this study, we investigated the role of TI in the pathogenesis of giant cell arteritis (GCA), a large-vessel vasculitis characterized by aberrant macrophage activation and excess cytokine production. Methods Monocytes from GCA patients and from age- and sex-matched healthy donors were subjected to polyfunctional studies, including cytokine production assays at baseline and following stimulation, intracellular metabolomics, chromatin immunoprecipitation-qPCR, and combined ATAC/RNA sequencing. Immunometabolic activation (i.e. glycolysis) was assessed in inflamed vessels of GCA patients with FDG-PET and immunohistochemistry (IHC), and the role of this pathway in sustaining cytokine production was confirmed with selective pharmacologic inhibition in GCA monocytes. Results GCA monocytes exhibited hallmark molecular features of TI. Specifically, these included enhanced IL-6 production upon stimulation, typical immunometabolic changes (e.g. increased glycolysis and glutaminolysis) and epigenetic changes promoting enhanced transcription of genes governing pro-inflammatory activation. Immunometabolic changes of TI (i.e. glycolysis) were a feature of myelomonocytic cells in GCA lesions and were required for enhanced cytokine production. Conclusions Myelomonocytic cells in GCA activate TI programs sustaining enhanced inflammatory activation with excess cytokine production. [ABSTRACT FROM AUTHOR]
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- 2023
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4. Oncogene-induced maladaptive activation of trained immunity in the pathogenesis and treatment of Erdheim-Chester disease
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Biavasco, Riccardo, primary, Molteni, Raffaella, additional, Stefanoni, Davide, additional, Nemkov, Travis, additional, Netea, Mihai G., additional, Domínguez-Andrés, Jorge, additional, Arts, Rob JW, additional, Merelli, Ivan, additional, Mazza, Davide, additional, Zambrano, Samuel, additional, Panigada, Maddalena, additional, Cantoni, Eleonora, additional, Tengesdal, Isak, additional, Maksud, Philippe, additional, Piras, Francesco, additional, De Luca, Giacomo, additional, Cassina, Laura, additional, Distefano, Gianfranco, additional, Loffreda, Alessia, additional, Gnani, Daniela, additional, Doglioni, Claudio, additional, Tomelleri, Alessandro, additional, Campochiaro, Corrado, additional, Joosten, Leo, additional, Dinarello, Charles A, additional, Kajaste-Rudnitski, Anna, additional, Haroche, Julien, additional, Cardaci, Simone, additional, Cenci, Simone, additional, Dagna, Lorenzo, additional, Ferrarini, Marina, additional, Ferrero, Elisabetta, additional, Boletta, Alessandra, additional, D'Alessandro, Angelo, additional, Montini, Eugenio, additional, and Cavalli, Giulio, additional
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- 2021
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5. Unraveling Pathophysiology and Hematopoiesis of Vexas Syndrome By Multi-Omics Analyses and Targeted Gene Editing
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Molteni, Raffaella, Fiumara, Martina, Campochiaro, Corrado, Tomelleri, Alessandro, Diral, Elisa, Varesi, Angelica, Weber, Alessandra, Stefanoni, Davide, Alfieri, Roberta, Albano, Luisa, Panigada, Maddalena, Cantoni, Eleonora, Canarutto, Daniele, Basso-Ricci, Luca, Quaranta, Pamela, D'Alessandro, Angelo, Matucci-Cerinic, Marco, Di Micco, Raffaella, Scala, Serena, Aiuti, Alessandro, Ciceri, Fabio, Merelli, Ivan, Dagna, Lorenzo, Cenci, Simone, Cavalli, Giulio, Naldini, Luigi, and Ferrari, Samuele
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- 2023
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6. The anti-inflammatory cytokine interleukin-37 is an inhibitor of trained immunity
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Cavalli, Giulio, primary, Tengesdal, Isak W., additional, Gresnigt, Mark, additional, Nemkov, Travis, additional, Arts, Rob J.W., additional, Domínguez-Andrés, Jorge, additional, Molteni, Raffaella, additional, Stefanoni, Davide, additional, Cantoni, Eleonora, additional, Cassina, Laura, additional, Giugliano, Silvia, additional, Schraa, Kiki, additional, Mills, Taylor S., additional, Pietras, Eric M., additional, Eisenmensser, Elan Z., additional, Dagna, Lorenzo, additional, Boletta, Alessandra, additional, D’Alessandro, Angelo, additional, Joosten, Leo A.B., additional, Netea, Mihai G., additional, and Dinarello, Charles A., additional
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- 2021
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7. Oncogene-induced maladaptive activation of trained immunity in the pathogenesis and treatment of Erdheim-Chester disease
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Molteni, Raffaella, Biavasco, Riccardo, Stefanoni, Davide, Nemkov, Travis, Domínguez-Andrés, Jorge, Arts, Rob J., Merelli, Ivan, Mazza, Davide, Zambrano, Samuel, Panigada, Maddalena, Cantoni, Eleonora, Tengesdal, Isak W., Maksud, Philippe, Piras, Francesco, Cesana, Daniela, Cassina, Laura, Distefano, Gianfranco, Loffreda, Alessia, Gnani, Daniela, De Luca, Giacomo, Tomelleri, Alessandro, Campochiaro, Corrado, Joosten, Leo A.B., Dinarello, Charles A., Kajaste-Rudnitski, Anna, Haroche, Julien, Cardaci, Simone, Cenci, Simone, Dagna, Lorenzo, Doglioni, Claudio, Ferrarini, Marina, Ferrero, Elisabetta, Boletta, Alessandra, D'Alessandro, Angelo, Montini, Eugenio, Netea, Mihai G., and Cavalli, Giulio
- Abstract
Trained immunity (TI) is a proinflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and is characterized by immunometabolic and epigenetic changes that enhance cytokine production. Maladaptive activation of TI (ie, in the absence of infection) may result in detrimental inflammation and development of disease; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined. In this study, we uncovered the oncogene-induced, maladaptive induction of TI in the pathogenesis of a human inflammatory myeloid neoplasm (Erdheim-Chester disease, [ECD]), characterized by the BRAFV600E oncogenic mutation in monocyte/macrophages and excess cytokine production. Mechanistically, myeloid cells expressing BRAFV600E exhibit all molecular features of TI: activation of the AKT/mammalian target of rapamycin signaling axis; increased glycolysis, glutaminolysis, and cholesterol synthesis; epigenetic changes on promoters of genes encoding cytokines; and enhanced cytokine production leading to hyperinflammatory responses. In patients with ECD, effective therapeutic strategies combat this maladaptive TI phenotype; in addition, pharmacologic inhibition of immunometabolic changes underlying TI (ie, glycolysis) effectively dampens cytokine production by myeloid cells. This study revealed the deleterious potential of inappropriate activation of TI in the pathogenesis of human inflammatory myeloid neoplasms and the opportunity for inhibition of TI in conditions characterized by maladaptive myeloid-driven inflammation.
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- 2021
- Full Text
- View/download PDF
8. Oncogene-induced maladaptive activation of trained immunity in the pathogenesis and treatment of Erdheim-Chester disease
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Mihai G. Netea, Riccardo Biavasco, Lorenzo Dagna, Simone Cenci, Travis Nemkov, Giulio Cavalli, Philippe Maksud, Claudio Doglioni, Gianfranco Distefano, Daniela Cesana, Charles A. Dinarello, Eleonora Cantoni, Anna Kajaste-Rudnitski, Corrado Campochiaro, Simone Cardaci, Daniela Gnani, Isak W. Tengesdal, Julien Haroche, Samuel Zambrano, Alessandro Tomelleri, Giacomo De Luca, Davide Stefanoni, Francesco Piras, Ivan Merelli, Angelo D'Alessandro, Maddalena Panigada, Davide Mazza, Rob J.W. Arts, Jorge Domínguez-Andrés, Alessia Loffreda, Laura Cassina, Raffaella Molteni, Eugenio Montini, Alessandra Boletta, Leo A. B. Joosten, Elisabetta Ferrero, Marina Ferrarini, Biavasco, Riccardo, Molteni, Raffaella, Stefanoni, Davide, Nemkov, Travi, Netea, Mihai G., Domínguez-Andrés, Jorge, Arts, Rob JW, Merelli, Ivan, Mazza, Davide, Zambrano, S, Panigada, Maddalena, Cantoni, Eleonora, Tengesdal, Isak, Maksud, Philippe, Piras, Francesco, De Luca, Giacomo, Cassina, Laura, Distefano, Gianfranco, Loffreda, Alessia, Gnani, Daniela, Doglioni, Claudio, Tomelleri, Alessandro, Campochiaro, Corrado, Joosten, Leo, Dinarello, Charles A, Kajaste-Rudnitski, Anna, Haroche, Julien, Cardaci, Simone, Cenci, Simone, Dagna, Lorenzo, Ferrarini, Marina, Ferrero, Elisabetta, Boletta, Alessandra, D'Alessandro, Angelo, Montini, Eugenio, and Cavalli, Giulio
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Proto-Oncogene Proteins B-raf ,Erdheim-Chester Disease ,Myeloid ,medicine.medical_treatment ,Immunology ,lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4] ,Inflammation ,Biochemistry ,Myeloid Neoplasm ,Proinflammatory cytokine ,Epigenesis, Genetic ,Pathogenesis ,medicine ,Humans ,Point Mutation ,Protein kinase B ,Cells, Cultured ,business.industry ,Monocyte ,Macrophages ,Immunity ,Cell Biology ,Hematology ,Oncogenes ,Cytokine ,medicine.anatomical_structure ,Cancer research ,medicine.symptom ,business - Abstract
Trained immunity (TI) is a proinflammatory program induced in monocyte/macrophages upon sensing of specific pathogens and is characterized by immunometabolic and epigenetic changes that enhance cytokine production. Maladaptive activation of TI (ie, in the absence of infection) may result in detrimental inflammation and development of disease; however, the exact role and extent of inappropriate activation of TI in the pathogenesis of human diseases is undetermined. In this study, we uncovered the oncogene-induced, maladaptive induction of TI in the pathogenesis of a human inflammatory myeloid neoplasm (Erdheim-Chester disease, [ECD]), characterized by the BRAFV600E oncogenic mutation in monocyte/macrophages and excess cytokine production. Mechanistically, myeloid cells expressing BRAFV600E exhibit all molecular features of TI: activation of the AKT/mammalian target of rapamycin signaling axis; increased glycolysis, glutaminolysis, and cholesterol synthesis; epigenetic changes on promoters of genes encoding cytokines; and enhanced cytokine production leading to hyperinflammatory responses. In patients with ECD, effective therapeutic strategies combat this maladaptive TI phenotype; in addition, pharmacologic inhibition of immunometabolic changes underlying TI (ie, glycolysis) effectively dampens cytokine production by myeloid cells. This study revealed the deleterious potential of inappropriate activation of TI in the pathogenesis of human inflammatory myeloid neoplasms and the opportunity for inhibition of TI in conditions characterized by maladaptive myeloid-driven inflammation.
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- 2021
9. La sociologia tra linguaggio e performatività
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CORBISIERO, Fabio, Fabio Corbisiero, Pietro Maturi, Luisa Amenta, Fatima Farina, Angela Genova, Paola Cantoni, Eleonora Caravello, Francesca Dragotto, Stefania Cavagnoli, Edith Cognigni, Claudia Santoni, Rita Fresu, Fabiana Fusco, Elisa Zanola, Dario Accolla, Valeria Bucchetti, Marta Isabella Reina, Giovanni Baule, Elena Caratti, Umberto Tolino, Chiara Cretelli, Inma Mora Sanchez, Mariano Gianola, Valentina Paola Cesarano, Milena Greco, Chiara Landi, Gaia Peruzzi, Luca Toschi, Fabio Corbisiero, Pietro Maturi, and Corbisiero, Fabio
- Abstract
Questa sezione del volume dedicata al rapporto tra sociologia, linguaggio e genere mira ad approfondire la riflessione sulle relazioni tra cambiamento socio-culturale ed evoluzione degli usi linguistici e comunicativi, partendo dall'idea che le parole possono, da un lato, marginalizzare ed emarginare; dall'altro lato, possono però diventare un efficace strumento della lotta alle disuguaglianze basate sul genere e sull'orientamento sessuale.
- Published
- 2016
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