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1. Dynamic changes in extracellular vesicle-associated miRNAs elicited by ultrasound in inflammatory bowel disease patients

Author

Tran, Florian, Scharmacher, Alena, Baran, Nathan, Mishra, Neha, Wozny, Marek, Chavez, Samuel Pineda, Bhardwaj, Archana, Hinz, Sophia, Juzenas, Simonas, Bernardes, Joana P., Sievers, Laura Katharina, Lessing, Matthias, Aden, Konrad, Lassen, Arne, Bergfeld, Arne, Weber, Hauke Jann, Neas, Lennart, Vetrano, Stefania, Schreiber, Stefan, and Rosenstiel, Philip

Published
2024
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2. Dysfunctional Extracellular Matrix Remodeling Supports Perianal Fistulizing Crohn′s Disease by a Mechanoregulated Activation of the Epithelial-to-Mesenchymal Transition

Author

Rizzo, Giulia, Rubbino, Federica, Elangovan, Sudharshan, Sammarco, Giusy, Lovisa, Sara, Restelli, Silvia, Pineda Chavez, Samuel Elias, Massimino, Luca, Lamparelli, Luigi, Paulis, Marianna, Maroli, Annalisa, Roda, Giulia, Shalaby, Mohammad, Carvello, Michele, Foppa, Caterina, Drummond, Sheona P., Spaggiari, Paola, Ungaro, Federica, Spinelli, Antonino, Malesci, Alberto, Repici, Alessandro, Day, Anthony J., Armuzzi, Alessandro, Danese, Silvio, and Vetrano, Stefania

Published
2023
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5. Dynamic Changes in Extracellular Vesicle-Associated miRNAs Elicited by Ultrasound in Inflammatory Bowel Disease Patients

Author

Tran, Florian, primary, Scharmacher, Alena, additional, Baran, Nathan, additional, Mishra, Neha, additional, Wozny, Marek, additional, Chavez, Samuel Pineda, additional, Bhardwaj, Archana, additional, Hinz, Sophia, additional, Juzenas, Simonas, additional, Bernardes, Joana P., additional, Sievers, Laura Katharina, additional, Lessing, Matthias, additional, Aden, Konrad, additional, Lassen, Arne, additional, Bergfeld, Arne, additional, Weber, Hauke Jann, additional, Neas, Lennart, additional, Vetrano, Stefania, additional, Schreiber, Stefan, additional, and Rosenstiel, Philip, additional

Published
2024
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11. Intestinal myofibroblast-specific Tpl2-Cox-2-PGE2 pathway links innate sensing to epithelial homeostasis

Author

Roulis, Manolis, Nikolaou, Christoforos, Kotsaki, Elena, Kaffe, Eleanna, Karagianni, Niki, Koliaraki, Vasiliki, Salpea, Klelia, Ragoussis, Jiannis, Aidinis, Vassilis, Martini, Eva, Becker, Christoph, Herschman, Harvey R, Vetrano, Stefania, Danese, Silvio, and Kollias, George

Subjects
Crohn's Disease, Inflammatory Bowel Disease, Autoimmune Disease, Digestive Diseases, Aetiology, Underpinning research, 1.1 Normal biological development and functioning, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Animals, Cell Lineage, Cell Proliferation, Colitis, Cyclooxygenase 2, Dextran Sulfate, Dinoprostone, Disease Susceptibility, Enzyme Activation, Epithelial Cells, Epithelium, Homeostasis, Humans, Immunity, Innate, Inflammation, Inflammatory Bowel Diseases, Intestines, MAP Kinase Kinase Kinases, Mice, Inbred C57BL, Models, Biological, Myofibroblasts, Phenotype, Proto-Oncogene Proteins, Signal Transduction, Crohn's disease, ulcerative colitis, mesenchymal cells, MAP kinases, cyclooxygenase-2
Abstract

Tumor progression locus-2 (Tpl2) kinase is a major inflammatory mediator in immune cell types recently found to be genetically associated with inflammatory bowel diseases (IBDs). Here we show that Tpl2 may exert a dominant homeostatic rather than inflammatory function in the intestine mediated specifically by subepithelial intestinal myofibroblasts (IMFs). Mice with complete or IMF-specific Tpl2 ablation are highly susceptible to epithelial injury-induced colitis showing impaired compensatory proliferation in crypts and extensive ulcerations without significant changes in inflammatory responses. Following epithelial injury, IMFs sense innate or inflammatory signals and activate, via Tpl2, the cyclooxygenase-2 (Cox-2)-prostaglandin E2 (PGE2) pathway, which we show here to be essential for the epithelial homeostatic response. Exogenous PGE2 administration rescues mice with complete or IMF-specific Tpl2 ablation from defects in crypt function and susceptibility to colitis. We also show that Tpl2 expression is decreased in IMFs isolated from the inflamed ileum of IBD patients indicating that Tpl2 function in IMFs may be highly relevant to human disease. The IMF-mediated mechanism we propose also involves the IBD-associated genes IL1R1, MAPK1, and the PGE2 receptor-encoding PTGER4. Our results establish a previously unidentified myofibroblast-specific innate pathway that regulates intestinal homeostasis and may underlie IBD susceptibility in humans.

Published
2014

12. IL-20 controls resolution of experimental colitis by regulating epithelial IFN/STAT2 signalling.

Author

Chiriac, Mircea Teodor, Hracsko, Zsuzsanna, Günther, Claudia, Gonzalez-Acera, Miguel, Atreya, Raja, Stolzer, Iris, Wittner, Leonie, Dressel, Anja, Schickedanz, Laura, Gamez-Belmonte, Reyes, Erkert, Lena, Hundorfean, Gheorghe, Zundler, Sebastian, Rath, Timo, Vetrano, Stefania, Danese, Silvio, Sturm, Gregor, Zlatko Trajanoski, Kühl, Anja A., and Siegmund, Britta

Subjects
KNOCKOUT mice, COLITIS, BIOCHEMISTRY, MEDICAL sciences, CELL adhesion molecules, INFLAMMATORY bowel diseases, ISCHEMIC colitis
Published
2024
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13. IL-20 controls resolution of experimental colitis by regulating epithelial IFN/STAT2 signalling

Author

Chiriac, Mircea Teodor, primary, Hracsko, Zsuzsanna, additional, Günther, Claudia, additional, Gonzalez-Acera, Miguel, additional, Atreya, Raja, additional, Stolzer, Iris, additional, Wittner, Leonie, additional, Dressel, Anja, additional, Schickedanz, Laura, additional, Gamez-Belmonte, Reyes, additional, Erkert, Lena, additional, Hundorfean, Gheorghe, additional, Zundler, Sebastian, additional, Rath, Timo, additional, Vetrano, Stefania, additional, Danese, Silvio, additional, Sturm, Gregor, additional, Trajanoski, Zlatko, additional, Kühl, Anja A, additional, Siegmund, Britta, additional, Hartmann, Arndt, additional, Wirtz, Stefan, additional, Siebler, Jürgen, additional, Finotto, Susetta, additional, Becker, Christoph, additional, and Neurath, Markus F, additional

Published
2023
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14. Proceedings of the signature series event of the international society for cellular therapy: “Advancements in cellular therapies and regenerative medicine in digestive diseases,” London, United Kingdom, May 3, 2017

Author

Ciccocioppo, Rachele, Dos Santos, Claudia C., Baumgart, Daniel C., Cangemi, Giuseppina C., Cardinale, Vincenzo, Ciacci, Carolina, De Coppi, Paolo, Haldar, Debashis, Klersy, Catherine, Nostro, M. Cristina, Ott, Michael, Piemonti, Lorenzo, Tomei, Alice A., Uygun, Basak, Vetrano, Stefania, and Orlando, Giuseppe

Published
2018
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16. Unveiling role of sphingosine-1-phosphate receptor 2 as a brake of epithelial stem cell proliferation and a tumor suppressor in colorectal cancer

Author

Petti, Luciana, Rizzo, Giulia, Rubbino, Federica, Elangovan, Sudharshan, Colombo, Piergiuseppe, Restelli, Silvia, Piontini, Andrea, Arena, Vincenzo, Carvello, Michele, Romano, Barbara, Cavalleri, Tommaso, Anselmo, Achille, Ungaro, Federica, D’Alessio, Silvia, Spinelli, Antonino, Stifter, Sanja, Grizzi, Fabio, Sgambato, Alessandro, Danese, Silvio, Laghi, Luigi, Malesci, Alberto, and Vetrano, Stefania

Published
2020
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19. Pomegranate Extract Affects Gut Biofilm Forming Bacteria and Promotes Intestinal Mucosal Healing Regulating the Crosstalk between Epithelial Cells and Intestinal Fibroblasts

Author

Rizzo, Giulia, primary, Pineda Chavez, Samuel Elias, additional, Vandenkoornhuyse, Elisa, additional, Cárdenas Rincón, Cindy Lorena, additional, Cento, Valeria, additional, Garlatti, Valentina, additional, Wozny, Marek, additional, Sammarco, Giusy, additional, Di Claudio, Alessia, additional, Meanti, Lisa, additional, Elangovan, Sudharshan, additional, Romano, Andrea, additional, Roda, Giulia, additional, Loy, Laura, additional, Dal Buono, Arianna, additional, Gabbiadini, Roberto, additional, Lovisa, Sara, additional, Rusconi, Roberto, additional, Repici, Alessandro, additional, Armuzzi, Alessandro, additional, and Vetrano, Stefania, additional

Published
2023
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20. Data from Protumor Steering of Cancer Inflammation by p50 NF-κB Enhances Colorectal Cancer Progression

Author

Porta, Chiara, primary, Ippolito, Alessandro, primary, Consonni, Francesca Maria, primary, Carraro, Lorenzo, primary, Celesti, Giuseppe, primary, Correale, Carmen, primary, Grizzi, Fabio, primary, Pasqualini, Fabio, primary, Tartari, Silvia, primary, Rinaldi, Maurizio, primary, Bianchi, Paolo, primary, Balzac, Fiorella, primary, Vetrano, Stefania, primary, Turco, Emilia, primary, Hirsch, Emilio, primary, Laghi, Luigi, primary, and Sica, Antonio, primary

Published
2023
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21. Table S2 from Protumor Steering of Cancer Inflammation by p50 NF-κB Enhances Colorectal Cancer Progression

Author

Porta, Chiara, primary, Ippolito, Alessandro, primary, Consonni, Francesca Maria, primary, Carraro, Lorenzo, primary, Celesti, Giuseppe, primary, Correale, Carmen, primary, Grizzi, Fabio, primary, Pasqualini, Fabio, primary, Tartari, Silvia, primary, Rinaldi, Maurizio, primary, Bianchi, Paolo, primary, Balzac, Fiorella, primary, Vetrano, Stefania, primary, Turco, Emilia, primary, Hirsch, Emilio, primary, Laghi, Luigi, primary, and Sica, Antonio, primary

Published
2023
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22. Supplementary materials and methods, figures and legends from Protumor Steering of Cancer Inflammation by p50 NF-κB Enhances Colorectal Cancer Progression

Author

Porta, Chiara, primary, Ippolito, Alessandro, primary, Consonni, Francesca Maria, primary, Carraro, Lorenzo, primary, Celesti, Giuseppe, primary, Correale, Carmen, primary, Grizzi, Fabio, primary, Pasqualini, Fabio, primary, Tartari, Silvia, primary, Rinaldi, Maurizio, primary, Bianchi, Paolo, primary, Balzac, Fiorella, primary, Vetrano, Stefania, primary, Turco, Emilia, primary, Hirsch, Emilio, primary, Laghi, Luigi, primary, and Sica, Antonio, primary

Published
2023
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23. Data from Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer

Author

Tacconi, Carlotta, primary, Ungaro, Federica, primary, Correale, Carmen, primary, Arena, Vincenzo, primary, Massimino, Luca, primary, Detmar, Michael, primary, Spinelli, Antonino, primary, Carvello, Michele, primary, Mazzone, Massimiliano, primary, Oliveira, Ana I., primary, Rubbino, Federica, primary, Garlatti, Valentina, primary, Spanò, Salvatore, primary, Lugli, Enrico, primary, Colombo, Federico S., primary, Malesci, Alberto, primary, Peyrin-Biroulet, Laurent, primary, Vetrano, Stefania, primary, Danese, Silvio, primary, and D’Alessio, Silvia, primary

Published
2023
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24. Figure S1 from Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer

Author

Tacconi, Carlotta, primary, Ungaro, Federica, primary, Correale, Carmen, primary, Arena, Vincenzo, primary, Massimino, Luca, primary, Detmar, Michael, primary, Spinelli, Antonino, primary, Carvello, Michele, primary, Mazzone, Massimiliano, primary, Oliveira, Ana I., primary, Rubbino, Federica, primary, Garlatti, Valentina, primary, Spanò, Salvatore, primary, Lugli, Enrico, primary, Colombo, Federico S., primary, Malesci, Alberto, primary, Peyrin-Biroulet, Laurent, primary, Vetrano, Stefania, primary, Danese, Silvio, primary, and D’Alessio, Silvia, primary

Published
2023
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25. Figure S5 and S6 from Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer

Author

Tacconi, Carlotta, primary, Ungaro, Federica, primary, Correale, Carmen, primary, Arena, Vincenzo, primary, Massimino, Luca, primary, Detmar, Michael, primary, Spinelli, Antonino, primary, Carvello, Michele, primary, Mazzone, Massimiliano, primary, Oliveira, Ana I., primary, Rubbino, Federica, primary, Garlatti, Valentina, primary, Spanò, Salvatore, primary, Lugli, Enrico, primary, Colombo, Federico S., primary, Malesci, Alberto, primary, Peyrin-Biroulet, Laurent, primary, Vetrano, Stefania, primary, Danese, Silvio, primary, and D’Alessio, Silvia, primary

Published
2023
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26. Figure S7-8 from Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer

Author

Tacconi, Carlotta, primary, Ungaro, Federica, primary, Correale, Carmen, primary, Arena, Vincenzo, primary, Massimino, Luca, primary, Detmar, Michael, primary, Spinelli, Antonino, primary, Carvello, Michele, primary, Mazzone, Massimiliano, primary, Oliveira, Ana I., primary, Rubbino, Federica, primary, Garlatti, Valentina, primary, Spanò, Salvatore, primary, Lugli, Enrico, primary, Colombo, Federico S., primary, Malesci, Alberto, primary, Peyrin-Biroulet, Laurent, primary, Vetrano, Stefania, primary, Danese, Silvio, primary, and D’Alessio, Silvia, primary

Published
2023
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27. Supplementary Data from Activation of the VEGFC/VEGFR3 Pathway Induces Tumor Immune Escape in Colorectal Cancer

Author

Tacconi, Carlotta, primary, Ungaro, Federica, primary, Correale, Carmen, primary, Arena, Vincenzo, primary, Massimino, Luca, primary, Detmar, Michael, primary, Spinelli, Antonino, primary, Carvello, Michele, primary, Mazzone, Massimiliano, primary, Oliveira, Ana I., primary, Rubbino, Federica, primary, Garlatti, Valentina, primary, Spanò, Salvatore, primary, Lugli, Enrico, primary, Colombo, Federico S., primary, Malesci, Alberto, primary, Peyrin-Biroulet, Laurent, primary, Vetrano, Stefania, primary, Danese, Silvio, primary, and D’Alessio, Silvia, primary

Published
2023
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28. The chemerin/CMKLR1 axis regulates intestinal graft-versus-host disease

Author

Dander, Erica, primary, Vinci, Paola, additional, Vetrano, Stefania, additional, Recordati, Camilla, additional, Piazza, Rocco, additional, Fazio, Grazia, additional, Bardelli, Donatella, additional, Bugatti, Mattia, additional, Sozio, Francesca, additional, Piontini, Andrea, additional, Bonanomi, Sonia, additional, Bertola, Luca, additional, Tassistro, Elena, additional, Valsecchi, Maria Grazia, additional, Calza, Stefano, additional, Vermi, William, additional, Biondi, Andrea, additional, Del Prete, Annalisa, additional, Sozzani, Silvano, additional, and D’Amico, Giovanna, additional

Published
2023
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29. The chemerin/CMKLR1 axis regulates intestinal graft-versus-host disease

Author

Dander, E, Vinci, P, Vetrano, S, Recordati, C, Piazza, R, Fazio, G, Bardelli, D, Bugatti, M, Sozio, F, Piontini, A, Bonanomi, S, Bertola, L, Tassistro, E, Valsecchi, M, Calza, S, Vermi, W, Biondi, A, Del Prete, A, Sozzani, S, D'Amico, G, Dander, Erica, Vinci, Paola, Vetrano, Stefania, Recordati, Camilla, Piazza, Rocco, Fazio, Grazia, Bardelli, Donatella, Bugatti, Mattia, Sozio, Francesca, Piontini, Andrea, Bonanomi, Sonia, Bertola, Luca, Tassistro, Elena, Valsecchi, Maria Grazia, Calza, Stefano, Vermi, William, Biondi, Andrea, Del Prete, Annalisa, Sozzani, Silvano, D'Amico, Giovanna, Dander, E, Vinci, P, Vetrano, S, Recordati, C, Piazza, R, Fazio, G, Bardelli, D, Bugatti, M, Sozio, F, Piontini, A, Bonanomi, S, Bertola, L, Tassistro, E, Valsecchi, M, Calza, S, Vermi, W, Biondi, A, Del Prete, A, Sozzani, S, D'Amico, G, Dander, Erica, Vinci, Paola, Vetrano, Stefania, Recordati, Camilla, Piazza, Rocco, Fazio, Grazia, Bardelli, Donatella, Bugatti, Mattia, Sozio, Francesca, Piontini, Andrea, Bonanomi, Sonia, Bertola, Luca, Tassistro, Elena, Valsecchi, Maria Grazia, Calza, Stefano, Vermi, William, Biondi, Andrea, Del Prete, Annalisa, Sozzani, Silvano, and D'Amico, Giovanna

Abstract

Gastrointestinal graft-versus-host disease (GvHD) is a major cause of mortality and morbidity following allogeneic bone marrow transplantation (allo-BMT). Chemerin is a chemotactic protein that recruits leukocytes to inflamed tissues by interacting with ChemR23/CMKLR1, a chemotactic receptor expressed by leukocytes, including macrophages. During acute GvHD, chemerin plasma levels were strongly increased in allo-BM-transplanted mice. The role of the chemerin/CMKLR1 axis in GvHD was investigated using Cmklr1-KO mice. WT mice transplanted with an allogeneic graft from Cmklr1-KO donors (t-KO) had worse survival and more severe GvHD. Histological analysis demonstrated that the gastrointestinal tract was the organ mostly affected by GvHD in t-KO mice. The severe colitis of t-KO mice was characterized by massive neutrophil infiltration and tissue damage associated with bacterial translocation and exacerbated inflammation. Similarly, Cmklr1- KO recipient mice showed increased intestinal pathology in both allogeneic transplant and dextran sulfate sodium-induced colitis. Notably, the adoptive transfer of WT monocytes into t-KO mice mitigated GvHD manifestations by decreasing gut inflammation and T cell activation. In patients, higher chemerin serum levels were predictive of GvHD development. Overall, these results suggest that CMKLR1/chemerin may be a protective pathway for the control of intestinal inflammation and tissue damage in GvHD.

Published
2023

30. ImmUniverse Consortium: Multi-omics integrative approach in personalized medicine for immune-mediated inflammatory diseases

Author

Vetrano, Stefania, Bouma, Gerben, Benschop, Robert J, Birngruber, Thomas, Costanzo, Antonio, D'Haens, GRAM, Frasca, Loredana, Hillenbrand, Rainer, Iversen, Lars, Johansen, Claus, Kaser, Arthur, Koenen, Hans JPM, Noehammer, Christa, Peyrin-Biroulet, Laurent, Raes, Jeroen, Ricotti, Leonardo, Rosenstiel, Philip, Satagopam, Venkata P, Schreiber, Stefan, Vermeire, Severine, Wollenberg, Andreas, Weidinger, Stephan, Ziemek, Daniel, Danese, Silvio, ImmUniverse Consortium, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Apollo - University of Cambridge Repository, Iversen, Lars [0000-0003-1816-4508], and Department of Bio-engineering Sciences

Subjects
Science & Technology, atopic dermatitis, liquid biopsy, FOS: Clinical medicine, Immunology, NK T-CELLS, Dermatitis, Atopic, All institutes and research themes of the Radboud University Medical Center, MICROBIOME, IL-13, immunomediated diseases, Inflammatory diseases Radboud Institute for Health Sciences [Radboudumc 5], LIPUS, Quality of Life, Disease Progression, Immunology and Allergy, Humans, dOFM, Precision Medicine, omic analyses, Life Sciences & Biomedicine, Inflammatory diseases Radboud Institute for Molecular Life Sciences [Radboudumc 5], POPULATION, Biomarkers, ulcerative colitis
Abstract

Peer reviewed: True, Immune mediated inflammatory diseases (IMIDs) are a heterogeneous group of debilitating, multifactorial and unrelated conditions featured by a dysregulated immune response leading to destructive chronic inflammation. The immune dysregulation can affect various organ systems: gut (e.g., inflammatory bowel disease), joints (e.g., rheumatoid arthritis), skin (e.g., psoriasis, atopic dermatitis), resulting in significant morbidity, reduced quality of life, increased risk for comorbidities, and premature death. As there are no reliable disease progression and therapy response biomarkers currently available, it is very hard to predict how the disease will develop and which treatments will be effective in a given patient. In addition, a considerable proportion of patients do not respond sufficiently to the treatment. ImmUniverse is a large collaborative consortium of 27 partners funded by the Innovative Medicine Initiative (IMI), which is sponsored by the European Union (Horizon 2020) and in-kind contributions of participating pharmaceutical companies within the European Federation of Pharmaceutical Industries and Associations (EFPIA). ImmUniverse aims to advance our understanding of the molecular mechanisms underlying two immune-mediated diseases, ulcerative colitis (UC) and atopic dermatitis (AD), by pursuing an integrative multi-omics approach. As a consequence of the heterogeneity among IMIDs patients, a comprehensive, evidence-based identification of novel biomarkers is necessary to enable appropriate patient stratification that would account for the inter-individual differences in disease severity, drug efficacy, side effects or prognosis. This would guide clinicians in the management of patients and represent a major step towards personalized medicine. ImmUniverse will combine the existing and novel advanced technologies, including multi-omics, to characterize both the tissue microenvironment and blood. This comprehensive, systems biology-oriented approach will allow for identification and validation of tissue and circulating biomarker signatures as well as mechanistic principles, which will provide information about disease severity and future disease progression. This truly makes the ImmUniverse Consortium an unparalleled approach.

Published
2022
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32. Centrally Determined Standardization of Flow Cytometry Methods Reduces Interlaboratory Variation in a Prospective Multicenter Study

Author

Westera, Liset, van Viegen, Tanja, Jeyarajah, Jenny, Azad, Azar, Bilsborough, Janine, van den Brink, Gijs R, Cremer, Jonathan, Danese, Silvio, DʼHaens, Geert, Eckmann, Lars, Faubion, William, Filice, Melissa, Korf, Hannelie, McGovern, Dermot, Panes, Julian, Salas, Azucena, Sandborn, William J, Silverberg, Mark S, Smith, Michelle I, Vermeire, Severine, Vetrano, Stefania, Shackelton, Lisa M, Stitt, Larry, Jairath, Vipul, Levesque, Barrett G, Spencer, David M, Feagan, Brian G, and Casteele, Niels Vande

Published
2017
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33. Rho-A prenylation and signaling link epithelial homeostasis to intestinal inflammation

Author

Lopez-Posadas, Rocio, Becker, Christoph, Gunther, Claudia, Tenzer, Stefan, Amann, Kerstin, Billmeier, Ulrike, Atreya, Raja, Fiorino, Gionata, Vetrano, Stefania, Danese, Silvio, Ekici, Arif B., Wirtz, Stefan, Thonn, Veronika, Watson, Alastair J.M., Brakebusch, Cord, Bergo, Martin, Neurath, Markus F., and Atreya, Imke

Subjects
Colorectal diseases -- Genetic aspects -- Development and progression, Cellular signal transduction -- Genetic aspects -- Health aspects, Genetic transcription -- Health aspects, Gastrointestinal diseases -- Genetic aspects -- Development and progression, Health care industry
Abstract

Although defects in intestinal barrier function are a key pathogenic factor in patients with inflammatory bowel iseases (IBDs), the molecular pathways driving disease-specific alterations of intestinal epithelial cells (IECs) are largely unknown. Here, we addressed this issue by characterizing the transcriptome of IECs from IBD patients using a genome-wide approach. We observed disease-specific alterations in IECs with markedly impaired Rho-A signaling in active IBD patients. Localization of epithelial Rho-A was shifted to the cytosol in IBDs, and inflammation was associated with suppressed Rho-A activation due to reduced expression of the Rho-A prenylation enzyme geranylgeranyltransferase-l (GGTase-I). Functionally, we found that mice with conditional loss of Rhoa or the gene encoding GGTase-I, Pggt1b, in IECs exhibit spontaneous chronic intestinal inflammation with accumulation of granulocytes and [CD4.sup.+] T cells. This phenotype was associated with cytoskeleton rearrangement and aberrant cell shedding, ultimately leading to loss of epithelial integrity and subsequent inflammation. These findings uncover deficient prenylation of Rho-A as a key player in the pathogenesis of IBDs. As therapeutic triggering of Rho-A signaling suppressed intestinal inflammation in mice with GGTase-I-deficient IECs, our findings suggest new avenues for treatment of epithelial injury and mucosal inflammation in IBD patients., Introduction Forming a mechanical boundary against pathogens, antigens, and toxins, the monolayer of intestinal epithelial cells (IECs) represents the human body's largest contact area with the environment (1). From their [...]

Published
2016
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36. Sa2026 LOW-INTENSITY PULSED ULTRASOUND REFLECTS THE STATUS OF MUCOSAL INJURY AND REPAIR THROUGH STAGE-SPECIFIC MIRNAS IN EXPERIMENTAL MODEL OF ULCERATIVE COLITIS

Author

Chavez, Samuel E. Pineda, Carriles, Alejandra A., Rizzo, Giulia, Wozny, Marek, Cafarelli, Andrea, Mori, Giada, Sorriento, Angela, Loy, Laura, Buono, Arianna Dal, Gabbiadini, Roberto, Bezzio, Cristina, Lucchetti, Donatella, Sgambato, Alessandro, Ricotti, Leonardo, Repici, Alessandro, Armuzzi, Alessandro, and Vetrano, Stefania

Published
2024
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37. Tu1179 LIPIDS DRIVE EPITHELIAL-MESENCHYMAL TRANSITION THROUGH THE ACTIVATION OF S1PR3 SIGNALING EXACERBATING INTESTINAL FIBROSIS IN CROHN'S DISEASE

Author

Rizzo, Giulia, Chavez, Samuel E. Pineda, Wozny, Marek, Mori, Giada, Carriles, Alejandra A., Ghisletti, Serena Maria Luisa, Gandolfi, Francesco, Vallelonga, Veronica, Paulis, Marianna, Grua, Angela La, Lovisa, Sara, Mazzarelli, Evelyn, Loy, Laura, Bezzio, Cristina, Spaggiari, Paola, Buono, Arianna Dal, Gabbiadini, Roberto, Carvello, Michele, Spinelli, Antonino, Repici, Alessandro, Armuzzi, Alessandro, and Vetrano, Stefania

Published
2024
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38. Tumor‐associated macrophages and risk of recurrence in stage III colorectal cancer

Author

Cavalleri, Tommaso, primary, Greco, Luana, additional, Rubbino, Federica, additional, Hamada, Tsuyoshi, additional, Quaranta, Maria, additional, Grizzi, Fabio, additional, Sauta, Elisabetta, additional, Craviotto, Vincenzo, additional, Bossi, Paola, additional, Vetrano, Stefania, additional, Rimassa, Lorenza, additional, Torri, Valter, additional, Bellazzi, Riccardo, additional, Mantovani, Alberto, additional, Ogino, Shuji, additional, Malesci, Alberto, additional, and Laghi, Luigi, additional

Published
2022
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41. Single-dose versus short-course prophylactic antibiotics for peroral endoscopic myotomy: a randomized controlled trial

Author

Maselli, Roberta, primary, Oliva, Alessandra, additional, Badalamenti, Matteo, additional, Galtieri, Piera Alessia, additional, Belletrutti, Paul James, additional, Spadaccini, Marco, additional, Nicoletti, Rosangela, additional, Finati, Elena, additional, Vetrano, Stefania, additional, Fosso, Federica, additional, Correale, Carmen, additional, Pellegatta, Gaia, additional, Hassan, Cesare, additional, and Repici, Alessandro, additional

Published
2021
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42. VEGF-C-dependent stimulation of lymphatic function ameliorates experimental inflammatory bowel disease

Author

D'Alessio, Silvia, Correale, Carmen, Tacconi, Carlotta, Gandelli, Alessandro, Pietrogrande, Giovanni, Vetrano, Stefania, Genua, Marco, Arena, Vincenzo, Spinelli, Antonino, Peyrin-Biroulet, Laurent, Fiocchi, Claudio, and Danese, Silvio

Subjects
Inflammatory bowel diseases -- Development and progression, Vascular endothelial growth factor -- Health aspects, Health care industry
Abstract

Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory bowel diseases (IBDs) of unknown etiology that are associated with an aberrant mucosal immune response. Neoangiogenesis and vascular injury are observed in IBD along with increased lymphangiogenesis. While the pathogenic role of angiogenesis in IBD is well characterized, it is not clear how or if increased lymphangiogenesis promotes disease. Here, we determined that enhancing lymphangiogenesis and lymphatic function reduces experimental IBD. Specifically, we demonstrated that adenoviral induction of prolymphangiogenic factor VEGF-C provides marked protection against the development of acute and chronic colitis in 2 different animal models. VEGF-C-dependent protection was observed in combination with increased inflammatory cell mobilization and bacterial antigen clearance from the inflamed colon to the draining lymph nodes. Moreover, we found that the VEGF-C/VEGFR3 pathway regulates macrophage (MΦ) plasticity and activation both in cultured MΦs and in vivo, imparting a hybrid M1-M2 phenotype. The protective function of VEGF-C was meditated by the so-called resolving MΦs during chronic experimental colitis in a STAT6-dependent manner. Together, these findings shed light on the contribution of lymphatics to the pathogenesis of gut inflammation and suggest that correction of defective lymphatic function with VEGF-C has potential as a therapeutic strategy for IBD., Introduction The inflammatory bowel diseases (IBDs), consisting of ulcerative colitis (UC) and Crohn's disease (CD), are characterized by chronic inflammation of the gastrointestinal tract in genetically susceptible individuals exposed to [...]

Published
2014
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49. GPR120 Prevents Colorectal Adenocarcinoma Progression by Sustaining The Mucosal Barrier Integrity

Author

Rubbino, Federica, primary, Garlatti, Valentina, additional, Garzarelli, Valeria, additional, Massimino, Luca, additional, Spanò, Salvatore, additional, Iadarola, Paolo, additional, Cagnone, Maddalena, additional, Giera, Martin, additional, Heijink, Marieke, additional, Guglielmetti, Simone, additional, Arena, Vincenzo, additional, Malesci, Alberto, additional, Laghi, Luigi, additional, Danese, Silvio, additional, and Vetrano, Stefania Stefania, additional

Published
2021
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