120 results on '"Turco, Fabio"'
Search Results
102. 728 Effect of Enteroglial-Derived S100B Protein on Human Peripheral and Mucosal Immune Cells' Functions
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Cirillo, Carla, primary, Sarnelli, Giovanni, additional, D'Aiuto, Elena, additional, Mango, Annamaria, additional, Turco, Fabio, additional, De Palma, Raffaele, additional, and Cuomo, Rosario, additional
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- 2010
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103. 201 Human Derived Enteroglial Cells Toll-Like Receptors mRNA Expression and Modulation by Pathogen and Probiotic Bacteria
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Turco, Fabio, primary, Cirillo, Carla, additional, Sarnelli, Giovanni, additional, Mango, Annamaria, additional, Cammarota, Marcella, additional, Giuliano, Mariateresa, additional, Cartenì, Maria, additional, and Cuomo, Rosario, additional
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- 2010
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104. Abstract 10418: Incidence and Variables Associated With Arrhythmias During Dobutamine-atropine Stress Echocardiography Among Patients With Chagas Disease.
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Rassi, Daniela C, Hotta, Viviane T, Furtado, Rogério G, Vieira, Marcelo Luiz C, Turco, Fabio P, Melato, Lucuano H, Dourado, Colandy N, Rassi, Luiz, and Rassi, Salvador
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- 2018
105. Corrigendum to 'What Experts Think About Prostate Cancer Management During the COVID-19 Pandemic: Report from the Advanced Prostate Cancer Consensus Conference 2021' [Eur Urol 82(1):6–11]
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Fabio Turco, Andrew Armstrong, Gerhardt Attard, Tomasz M. Beer, Himisha Beltran, Anders Bjartell, Alberto Bossi, Alberto Briganti, Rob G. Bristow, Muhammad Bulbul, Orazio Caffo, Kim N. Chi, Caroline Clarke, Noel Clarke, Ian D. Davis, Johann de Bono, Ignacio Duran, Ros Eeles, Eleni Efstathiou, Jason Efstathiou, Christopher P. Evans, Stefano Fanti, Felix Y. Feng, Karim Fizazi, Mark Frydenberg, Dan George, Martin Gleave, Susan Halabi, Daniel Heinrich, Celestia Higano, Michael S. Hofman, Maha Hussain, Nicholas James, Rob Jones, Ravindran Kanesvaran, Raja B. Khauli, Laurence Klotz, Raya Leibowitz, Christopher Logothetis, Fernando Maluf, Robin Millman, Alicia K. Morgans, Michael J. Morris, Nicolas Mottet, Hind Mrabti, Declan G. Murphy, Vedang Murthy, William K. Oh, Onyeanunam Ngozi Ekeke, Piet Ost, Joe M. O'Sullivan, Anwar R. Padhani, Christopher Parker, Darren M.C. Poon, Colin C. Pritchard, Danny M. Rabah, Dana Rathkopf, Robert E. Reiter, Mark Rubin, Charles J. Ryan, Fred Saad, Juan Pablo Sade, Oliver Sartor, Howard I. Scher, Neal Shore, Iwona Skoneczna, Eric Small, Matthew Smith, Howard Soule, Daniel Spratt, Cora N. Sternberg, Hiroyoshi Suzuki, Christopher Sweeney, Matthew Sydes, Mary-Ellen Taplin, Derya Tilki, Bertrand Tombal, Levent Türkeri, Hiroji Uemura, Hirotsugu Uemura, Inge van Oort, Kosj Yamoah, Dingwei Ye, Almudena Zapatero, Silke Gillessen, Aurelius Omlin, Turco, Fabio, Armstrong, Andrew, Attard, Gerhardt, Beer, Tomasz M, Beltran, Himisha, Bjartell, Ander, Bossi, Alberto, Briganti, Alberto, Bristow, Rob G, Bulbul, Muhammad, Caffo, Orazio, Chi, Kim N, Clarke, Caroline, Clarke, Noel, Davis, Ian D, de Bono, Johann, Duran, Ignacio, Eeles, Ro, Efstathiou, Eleni, Efstathiou, Jason, Evans, Christopher P, Fanti, Stefano, Feng, Felix Y, Fizazi, Karim, Frydenberg, Mark, George, Dan, Gleave, Martin, Halabi, Susan, Heinrich, Daniel, Higano, Celestia, Hofman, Michael S, Hussain, Maha, James, Nichola, Jones, Rob, Kanesvaran, Ravindran, Khauli, Raja B, Klotz, Laurence, Leibowitz, Raya, Logothetis, Christopher, Maluf, Fernando, Millman, Robin, Morgans, Alicia K, Morris, Michael J, Mottet, Nicola, Mrabti, Hind, Murphy, Declan G, Murthy, Vedang, Oh, William K, Ekeke, Onyeanunam Ngozi, Ost, Piet, O'Sullivan, Joe M, Padhani, Anwar R, Parker, Christopher, Poon, Darren M C, Pritchard, Colin C, Rabah, Danny M, Rathkopf, Dana, Reiter, Robert E, Rubin, Mark, Ryan, Charles J, Saad, Fred, Sade, Juan Pablo, Sartor, Oliver, Scher, Howard I, Shore, Neal, Skoneczna, Iwona, Small, Eric, Smith, Matthew, Soule, Howard, Spratt, Daniel, Sternberg, Cora N, Suzuki, Hiroyoshi, Sweeney, Christopher, Sydes, Matthew, Taplin, Mary-Ellen, Tilki, Derya, Tombal, Bertrand, Türkeri, Levent, Uemura, Hiroji, Uemura, Hirotsugu, van Oort, Inge, Yamoah, Kosj, Ye, Dingwei, Zapatero, Almudena, Gillessen, Silke, and Omlin, Aurelius
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Urology ,Prostate cancer Prostate cancer management COVID-19 pandemic COVID-19 vaccine COVID-19 boost injection Telemedicine - Abstract
Patients with advanced prostate cancer (APC) may be at greater risk for severe illness, hospitalisation, or death from coronavirus disease 2019 (COVID-19) due to male gender, older age, potential immunosuppressive treatments, or comorbidities. Thus, the optimal management of APC patients during the COVID-19 pandemic is complex. In October 2021, during the Advanced Prostate Cancer Consensus Conference (APCCC) 2021, the 73 voting members of the panel members discussed and voted on 13 questions on this topic that could help clinicians make treatment choices during the pandemic. There was a consensus for full COVID-19 vaccination and booster injection in APC patients. Furthermore, the voting results indicate that the expert’s treatment recommendations are influenced by the vaccination status: the COVID-19 pandemic altered management of APC patients for 70% of the panellists before the vaccination was available but only for 25% of panellists for fully vaccinated patients. Most experts (71%) were less likely to use docetaxel and abiraterone in unvaccinated patients with metastatic hormone-sensitive prostate cancer. For fully vaccinated patients with high-risk localised prostate cancer, there was a consensus (77%) to follow the usual treatment schedule, whereas in unvaccinated patients, 55% of the panel members voted for deferring radiation therapy. Finally, there was a strong consensus for the use of telemedicine for monitoring APC patients. Patient summary In the Advanced Prostate Cancer Consensus Conference 2021, the panellists reached a consensus regarding the recommendation of the COVID-19 vaccine in prostate cancer patients and use of telemedicine for monitoring these patients.
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- 2022
106. Molecular Signaling and Dysfunction of the Human Reactive Enteric Glial Cell Phenotype
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Bradley Needleman, Iveta Grants, Rosario Cuomo, Andrómeda Liñán-Rico, Alan Harzman, Fabio Turco, Emmett E. Whitaker, Razvan Arsenescu, Paolo Fadda, Fievos L. Christofi, Fernando Ochoa-Cortes, Mahmoud Abdel-Rasoul, Liñán Rico, Andromeda, Turco, Fabio, Ochoa Cortes, Fernando, Harzman, Alan, Needleman, Bradley J, Arsenescu, Razvan, Abdel Rasoul, Mahmoud, Fadda, Paolo, Grants, Iveta, Whitaker, Emmett, Cuomo, Rosario, and Christofi, Fievos L.
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Lipopolysaccharides ,0301 basic medicine ,Gastrointestinal Diseases ,Vesicular Transport Proteins ,Gene Expression ,Nitric Oxide Synthase Type II ,Tryptophan Hydroxylase ,Mechanotransduction, Cellular ,Inflammatory bowel disease ,Enteric Nervous System ,Adenosine Triphosphate ,Immunology and Allergy ,Receptor ,Cells, Cultured ,Irritable bowel syndrome ,Caspase 3 ,digestive, oral, and skin physiology ,Receptors, Purinergic ,Gastroenterology ,Phenotype ,Up-Regulation ,Jejunum ,Cytokines ,Intercellular Signaling Peptides and Proteins ,Animal studies ,medicine.symptom ,Signal transduction ,Neuroglia ,Signal Transduction ,enteric glia cell, inflammatory bowel disease, gastrointestinal disorders ,Motility ,Inflammation ,S100 Calcium Binding Protein beta Subunit ,Biology ,Article ,Interferon-gamma ,03 medical and health sciences ,Colon, Sigmoid ,parasitic diseases ,medicine ,Humans ,Superoxide Dismutase ,Granulocyte-Macrophage Colony-Stimulating Factor ,medicine.disease ,digestive system diseases ,030104 developmental biology ,Immunology ,Calcium ,Calcium Channels ,Carrier Proteins ,Gastrointestinal Motility ,Heme Oxygenase-1 ,Transcription Factors - Abstract
BACKGROUND: Clinical observations or animal studies implicate enteric glial cells in motility disorders, irritable bowel syndrome, inflammatory bowel disease, gastrointestinal (GI) infections, postoperative ileus, and slow transit constipation. Mechanisms underlying glial responses to inflammation in human GI tract are not understood. Our goal was to identify the "reactive human enteric glial cell (rhEGC) phenotype" induced by inflammation, and probe its functional relevance. METHODS: Human enteric glial cells in culture from 15 GI-surgical specimens were used to study gene expression, Ca, and purinergic signaling by Ca/fluo-4 imaging and mechanosensitivity. A nanostring panel of 107 genes was designed as a read out of inflammation, transcription, purinergic signaling, vesicular transport protein, channel, antioxidant, and other pathways. A 24-hour treatment with lipopolysaccharide (200 μg/mL) and interferon-γ (10 μg/mL) was used to induce inflammation and study molecular signaling, flow-dependent Ca responses from 3 mL/min to 10 mL/min, adenosine triphosphate (ATP) release, and ATP responses. RESULTS: Treatment induced a "rhEGC phenotype" and caused up-regulation in messenger RNA transcripts of 58% of 107 genes analyzed. Regulated genes included inflammatory genes (54%/IP10; IFN-γ; CxCl2; CCL3; CCL2; C3; s100B; IL-1β; IL-2R; TNF-α; IL-4; IL-6; IL-8; IL-10; IL-12A; IL-17A; IL-22; and IL-33), purine-genes (52%/AdoR2A; AdoR2B; P2RY1; P2RY2; P2RY6; P2RX3; P2RX7; AMPD3; ENTPD2; ENTPD3; and NADSYN1), channels (40%/Panx1; CHRNA7; TRPV1; and TRPA1), vesicular transporters (SYT1, SYT2, SNAP25, and SYP), transcription factors (relA/relB, SOCS3, STAT3, GATA_3, and FOXP3), growth factors (IGFBP5 and GMCSF), antioxidant genes (SOD2 and HMOX1), and enzymes (NOS2; TPH2; and CASP3) (P < 0.0001). Treatment disrupted Ca signaling, ATP, and mechanical/flow-dependent Ca responses in human enteric glial cells. ATP release increased 5-fold and s100B decreased 33%. CONCLUSIONS: The "rhEGC phenotype" is identified by a complex cascade of pro-inflammatory pathways leading to alterations of important molecular and functional signaling pathways (Ca, purinergic, and mechanosensory) that could disrupt GI motility. Inflammation induced a "purinergic switch" from ATP to adenosine diphosphate/adenosine/uridine triphosphate signaling. Findings have implications for GI infection, inflammatory bowel disease, postoperative ileus, motility, and GI disorders.
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- 2016
107. Enteric Glial Cells: A New Frontier in Neurogastroenterology and Clinical Target for Inflammatory Bowel Diseases
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Suren Soghomonyan, Sven Wehner, Fernando Ochoa-Cortes, Rosario Cuomo, Fabio Turco, Andrómeda Liñán-Rico, Emmett E. Whitaker, Fievos L. Christofi, Ochoa Cortes, Fernando, Turco, Fabio, Linan Rico, Andromeda, Soghomonyan, Suren, Whitaker, Emmett, Wehner, Sven, Cuomo, Rosario, and Christofi, Fievos L.
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0301 basic medicine ,Cell signaling ,Central nervous system ,reactive hEGC phenotype ,Inflammation ,tipartite synapse ,Cell Communication ,Biology ,calcium signaling ,Enteric Nervous System ,postoperative ileus ,03 medical and health sciences ,chemistry.chemical_compound ,human enteric glial cell ,GI infection ,neuroglial communication ,medicine ,Immunology and Allergy ,Humans ,Future Directions and Methods for IBD Research ,Palmitoylethanolamide ,Inflammatory Bowel Disease ,Gastroenterology ,Purinergic signalling ,Neurogastroenterology ,Inflammatory Bowel Diseases ,Prognosis ,gliotransmission ,3. Good health ,030104 developmental biology ,medicine.anatomical_structure ,enteric glial cells ,chemistry ,motility ,Cytoprotection ,Immunology ,Neuroglia ,Enteric nervous system ,medicine.symptom ,Enteric Glia ,Neuroscience ,purinergic signaling ,Signal Transduction - Abstract
Article first Published online 18 December 2015, The word “glia” is derived from the Greek word “γλοια,” glue of the enteric nervous system, and for many years, enteric glial cells (EGCs) were believed to provide mainly structural support. However, EGCs as astrocytes in the central nervous system may serve a much more vital and active role in the enteric nervous system, and in homeostatic regulation of gastrointestinal functions. The emphasis of this review will be on emerging concepts supported by basic, translational, and/or clinical studies, implicating EGCs in neuron-to-glial (neuroglial) communication, motility, interactions with other cells in the gut microenvironment, infection, and inflammatory bowel diseases. The concept of the “reactive glial phenotype” is explored as it relates to inflammatory bowel diseases, bacterial and viral infections, postoperative ileus, functional gastrointestinal disorders, and motility disorders. The main theme of this review is that EGCs are emerging as a new frontier in neurogastroenterology and a potential therapeutic target. New technological innovations in neuroimaging techniques are facilitating progress in the field, and an update is provided on exciting new translational studies. Gaps in our knowledge are discussed for further research. Restoring normal EGC function may prove to be an efficient strategy to dampen inflammation. Probiotics, palmitoylethanolamide (peroxisome proliferator-activated receptor–α), interleukin-1 antagonists (anakinra), and interventions acting on nitric oxide, receptor for advanced glycation end products, S100B, or purinergic signaling pathways are relevant clinical targets on EGCs with therapeutic potential.
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- 2015
108. Bacterial stimuli activate nitric oxide colonic mucosal production in diverticular disease. Protective effects ofL. casei DG® (Lactobacillus paracaseiCNCM I-1572)
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F.P. Zito, Rosario Cuomo, Giovanni Domenico De Palma, Giovanni Sarnelli, Martina Cargiolli, Paolo Andreozzi, Fabio Turco, Nicola Gennarelli, Walter Fiore, Ilaria Palumbo, Turco, Fabio, Andreozzi, Paolo, Palumbo, Ilaria, Zito, FRANCESCO PAOLO, Cargiolli, Martina, Fiore, Walter, Gennarelli, Nicola, DE PALMA, GIOVANNI DOMENICO, Sarnelli, Giovanni, and Cuomo, Rosario
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0301 basic medicine ,Lactobacillus paracasei ,Gut flora ,digestive system ,diverticular disease, probiotics, nitric oxide, human colonic mucosa ,Microbiology ,Nitric oxide ,law.invention ,Pathogenesis ,03 medical and health sciences ,chemistry.chemical_compound ,Probiotic ,0302 clinical medicine ,law ,Medicine ,skin and connective tissue diseases ,biology ,business.industry ,digestive, oral, and skin physiology ,Gastroenterology ,Original Articles ,biology.organism_classification ,030104 developmental biology ,Oncology ,chemistry ,Immunology ,Diverticular disease ,030211 gastroenterology & hepatology ,sense organs ,business - Abstract
Background: Micro-inflammation and changes in gut microbiota may play a role in the pathogenesis of diverticular disease (DD). Objective: The objective of this article is to evaluate the expression of nitric oxide (NO)-related mediators and S100B in colonic mucosa of patients with DD in an ex vivo model of bacterial infection. Methods: Intestinal biopsies obtained from patients with diverticulosis, symptomatic uncomplicated diverticular disease (SUDD) and SUDD with previous acute diverticulitis (SUDD+AD) were stimulated with the probiotic L. casei DG® (LCDG) and/or the pathogen enteroinvasive Escherichia coli (EIEC). S100B, NO release and iNOS expression were then evaluated. Results: Basal iNOS expression was significantly increased in SUDD and SUDD+AD patients. Basal NO expression was significantly increased in SUDD+AD. No differences in S100B release were found. In all groups, iNOS expression was significantly increased by EIEC and reduced by LCDG. In all groups, except for SUDD+AD, EIEC significantly increased NO release, whereas no increase was observed when LCDG was added to biopsies. EIEC did not induce significant changes in S100B release. Conclusions: Colonic mucosa of patients with DD is characterized by a different reactivity toward pathogenic stimuli. LCDG plays a role in counteracting the pro-inflammatory effects exerted by EIEC, suggesting a beneficial role of this probiotic in DD.
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- 2017
109. Palmitoylethanolamide improves colon inflammation through an enteric glia/toll like receptor 4-dependent PPAR-α activation
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Fabio Turco, Jie Lu, Luca Steardo, Giuseppe Esposito, Antonio Steardo, Ilaria Palumbo, Rosario Cuomo, Giovanni Sarnelli, Elena Capoccia, Esposito, G, Capoccia, E, Turco, Fabio, Palumbo, Ilaria, Lu, J, Steardo, A, Cuomo, Rosario, Sarnelli, Giovanni, and Steardo, L.
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Male ,Indoles ,Nitric Oxide Synthase Type II ,Peroxisome proliferator-activated receptor ,Severity of Illness Index ,Mice ,chemistry.chemical_compound ,ENTERIC NERVOUS SYSTEM ,Anilides ,Cells, Cultured ,chemistry.chemical_classification ,Toll-like receptor ,Anti-Inflammatory Agents, Non-Steroidal ,Dextran Sulfate ,NF-kappa B ,Gastroenterology ,Middle Aged ,Colitis ,Neutrophil Infiltration ,Ethanolamines ,Female ,Tumor necrosis factor alpha ,medicine.symptom ,Neuroglia ,Signal Transduction ,NERVOUS CONTROL OF INTESTINAL FUNCTIONS ,Nerve Tissue Proteins ,Inflammation ,Palmitic Acids ,S100 Calcium Binding Protein beta Subunit ,Biology ,Nitric Oxide ,Dinoprostone ,Proinflammatory cytokine ,Colon, Sigmoid ,Glial Fibrillary Acidic Protein ,GUT INFLAMMATION ,medicine ,Animals ,Humans ,PPAR alpha ,ulcerative colitis ,Palmitoylethanolamide ,Tumor Necrosis Factor-alpha ,nervous control of intestinal functions ,enteric nervous system ,gut inflammation ,Rectum ,medicine.disease ,Amides ,PPAR gamma ,Toll-Like Receptor 4 ,chemistry ,Cyclooxygenase 2 ,Immunology ,Cancer research ,TLR4 ,Colitis, Ulcerative ,Endocannabinoids - Abstract
Objective Enteric glia activation has been reported to amplify intestinal inflammation via the enteroglial-specific S100B protein. This neurotrophin promotes macrophage recruitment in the mucosa, amplify colonic inflammation and interacts with toll-like receptors (TLR). Molecules inhibiting S100B-driven enteric activation might mitigate the course of ulcerative colitis (UC). This study aims to investigate the effects of palmitoylethanolammide (PEA), a drug able to counteract astroglial activation in the central nervous system, on intestinal inflammation, in humans and mice. Design Mouse models of dextran sodium sulphate (DSS)-induced colitis, colonic biopsies deriving from UC patients and primary cultures of mouse and human enteric glial cells (EGC), have been used to assess the effects of PEA, alone or in the presence of specific PPARα or PPARγ antagonists, on: macroscopic signs of UC (DAI score, colon length, spleen weight, macrophages/neutrophils infiltration); the expression and release of proinflammatory markers typical of UC; TLR pathway in EGCs. Results PEA treatment improves all macroscopic signs of UC and decreases the expression and release of all the proinflammatory markers tested. PEA anti-inflammatory effects are mediated by the selective targeting of the S100B/TLR4 axis on ECG, causing a downstream inhibition of nuclear factor kappa B (NF-kB)-dependent inflammation. Antagonists at PPARα, but not PPARγ, abolished PEA effects, in mice and in humans. Conclusions Because of its lack of toxicity, its ability in reducing inflammation and its selective PPARα action, PEA might be an innovative molecule to broaden pharmacological strategies against UC.
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- 2013
110. Acetonic extract from the feijoa sellowiana berg. fruit exerts antioxidant properties and modulates disaccharidases activities in human intestinal epithelial cells
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Fabio, Turco, Ilaria, Palumbo, Paolo, Andreozzi, Giovanni, Sarnelli, Francesca, De Ruberto, Giuseppe, Esposito, Adriana, Basile, Rosario, Cuomo, Turco, Fabio, Palumbo, Ilaria, Andreozzi, Paolo, Sarnelli, Giovanni, De Ruberto, Francesca, Esposito, Giuseppe, Basile, Adriana, and Cuomo, Rosario
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Pharmacology ,Plant Extracts ,Feijoa Sellowiana ,proliferation ,Functional food ,Epithelial Cells ,Disaccharidases ,Antioxidants ,Lactose malabsorption ,Feijoa ,Sucrase-isomaltase deficiency ,HT-29 cells ,Fruit ,Humans ,Oxidative stre ,Disaccharidases deficiency ,Intestinal Mucosa - Abstract
Feijoa sellowiana fruit has been shown to possess various biological activities, such as anti-bacterial and anti-cancer properties, in a variety of cellular models, but its activity on human intestinal epithelial cells has never been tested. The purpose of this study was to investigate the effects of the acetonic extract of F. sellowiana fruits on the viability, membrane peroxidation, disaccharidases activities and proliferation of in vitro models of human intestinal epithelial cells. To obtain this goal, Caco-2 and HT-29 cells were exposed to the acetonic extract for 24 h. Cell proliferation, viability, lactase and sucrase-isomaltase activity and H2 O2 -induced membrane lipid peroxidation were tested. We found that, compared to control conditions, the acetonic extract significantly increased lactase and sucrase-isomaltase activity in Caco-2, but not HT-29, cells, decreased proliferation, had no effects on viability and restored lipid peroxidation in both cell models. This study suggests that the acetonic extract improves lactase and sucrase-isomaltase activity, inhibits cell proliferation, have no cytotoxic effects and prevent lipid peroxidation of intestinal epithelial cells. These effects may be exploited in case of disaccharidases deficit and also as an adjuvant treatment of diseases related to oxidative stress. Copyright © 2016 John WileySons, Ltd.
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- 2016
111. The bitter taste receptor agonist quinine reduces calorie intake and increases the postprandial release of cholecystokinin in healthy subjects
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Viviana Verlezza, Alessandra D Alessandro, Fabio Turco, Rosario Cuomo, Marcella Pesce, F.P. Zito, Paolo Andreozzi, Giovanni Sarnelli, Ilaria Palumbo, Katherine Esposito, Andreozzi, Paolo, Sarnelli, Giovanni, Pesce, Marcella, Zito, Francesco P., D'Alessandro, Alessandra, Verlezza, Viviana, Palumbo, Ilaria, Turco, Fabio, Esposito, Katherine, Cuomo, Rosario, and Zito, FRANCESCO PAOLO
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medicine.medical_specialty ,Quinine ,Taste ,Meal ,Calorie ,business.industry ,digestive, oral, and skin physiology ,Gastroenterology ,Placebo ,Ghrelin ,Endocrinology ,Postprandial ,Food intake ,Internal medicine ,medicine ,Original Article ,Neurology (clinical) ,business ,Cholecystokinin ,medicine.drug - Abstract
Background/Aims Bitter taste receptors are expressed throughout the digestive tract. Data on animals have suggested these receptors are involved in the gut hormone release, but no data are available in humans. Our aim is to assess whether bitter agonists influence food intake and gut hormone release in healthy subjects. Methods Twenty healthy volunteers were enrolled in a double-blind cross-over study. On 2 different days, each subject randomly received an acid-resistant capsule containing either placebo or 18 mg of hydrochloride (HCl) quinine. After 60 minutes, all subjects were allowed to eat an ad libitum meal until satiated. Plasma samples were obtained during the experiment in order to evaluate cholecystokinin (CCK) and ghrelin levels. Each subject was screened to determine phenylthiocarbamide (PTC) tasting status. Results Calorie intake was significantly lower when subjects received HCl quinine than placebo (514 ± 248 vs 596 ± 286 kcal; P = 0.007). Significantly higher CCK ΔT90 vs T0 and ΔT90 vs T60 were found when subjects received HCl quinine than placebo (0.70 ± 0.69 vs 0.10 ± 0.86 ng/mL, P = 0.026; 0.92 ± 0.75 vs 0.50 ± 0.55 ng/mL, P = 0.033, respectively). PTC tasters ingested a significantly lower amount of calories when they received HCl quinine compared to placebo (526 ± 275 vs 659 ± 320 kcal; P = 0.005), whereas no significant differences were found for PTC non-tasters (499 ± 227 vs 519 ± 231 kcal; P = 0.525). Conclusions This study showed that intra-duodenal release of a bitter compound is able to significantly affect calorie intake and CCK release after a standardized meal. Our results suggest that bitter taste receptor signaling may have a crucial role in the control of food intake.
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- 2015
112. S100B protein in the gut: The evidence for enteroglial-sustained intestinal inflammation
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Rosario Cuomo, Fabio Turco, Carla Cirillo, Luca Steardo, Giuseppe Esposito, Giovanni Sarnelli, Cirillo, Carla, Sarnelli, Giovanni, Esposito, G, Turco, Fabio, Steardo, L, and Cuomo, Rosario
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Central Nervous System ,Enteric glia ,Central nervous system ,Inflammation ,Review ,S100 Calcium Binding Protein beta Subunit ,Nitric Oxide ,enetric nervous system ,intestinal inflammation ,Glial Fibrillary Acidic Protein ,medicine ,Extracellular ,Animals ,Humans ,nitric oxide ,intestinal diseases ,enteric glial cells ,Nerve Growth Factors ,Intestinal Mucosa ,Glial fibrillary acidic protein ,biology ,Microglia ,S100 Proteins ,Gastroenterology ,Brain ,General Medicine ,Intestinal Diseases ,medicine.anatomical_structure ,Nerve growth factor ,Astrocytes ,Immunology ,biology.protein ,Neuroglia ,medicine.symptom ,Immunosuppressive Agents - Abstract
Glial cells in the gut represent the morphological and functional equivalent of astrocytes and microglia in the central nervous system (CNS). In recent years, the role of enteric glial cells (EGCs) has extended from that of simple nutritive support for enteric neurons to that of being pivotal participants in the regulation of inflammatory events in the gut. Similar to the CNS astrocytes, the EGCs physiologically express the S100B protein that exerts either trophic or toxic effects depending on its concentration in the extracellular milieu. In the CNS, S100B overexpression is responsible for the initiation of a gliotic reaction by the release of pro-inflammatory mediators, which may have a deleterious effect on neighboring cells. S100B-mediated pro-inflammatory effects are not limited to the brain: S100B overexpression is associated with the onset and maintenance of inflammation in the human gut too. In this review we describe the major features of EGCs and S100B protein occurring in intestinal inflammation deriving from such.
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- 2011
113. Hormonal Agents in Localized and Advanced Prostate Cancer: Current Use and Future Perspectives.
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Turco F, Buttigliero C, Delcuratolo MD, Gillessen S, Vogl UM, Zilli T, Fossati N, Gallina A, Farinea G, Di Stefano RF, Calabrese M, Saporita I, Crespi V, Poletto S, Palesandro E, Di Maio M, Scagliotti GV, and Tucci M
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- Humans, Male, Antineoplastic Agents, Hormonal therapeutic use, Receptors, Androgen metabolism, Treatment Outcome, Prostatic Neoplasms drug therapy, Prostatic Neoplasms pathology, Prostatic Neoplasms metabolism, Androgen Receptor Antagonists therapeutic use, Androgen Antagonists therapeutic use
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Prostate cancer (PC) is generally a hormone-dependent tumor. Androgen deprivation therapy ( has been the standard of care in metastatic disease for more than 80 years. Subsequent studies have highlighted the efficacy of ADT even in earlier disease settings such as in localized disease or in the case of biochemical recurrence (BCR). Improved knowledge of PC biology and ADT resistance mechanisms have led to the development of novel generation androgen receptor pathway inhibitors (ARPI). Initially used only in patients who became resistant to ADT, ARPI have subsequently shown to be effective when used in patients with metastatic hormone-naive disease and in recent years their effectiveness has also been evaluated in localized disease and in case of BCR. The objective of this review is to describe the current role of agents interfering with the androgen receptor in different stages of PC and to point out future perspectives., Competing Interests: Disclosure Fabio Turco: Travel support: Bayer. Silke Gillessen: (last 3 years) personal honoraria for participation in advisory boards from Amgen, MSD; other honoraria from Radio-televisione Svizzera Italiana (RSI), German-speaking European School of Oncology (DESO); invited speaker for ESMO, Swiss group for Clinical Cancer Research (SAKK), Swiss Academy of Multidisciplinary oncology (SAMO), Orikata academy research group, China Anticancer Association Genitourinary Oncology Committee (CACA-GU); Speaker's bureau for Janssen Cilag; travel grant from ProteoMEdiX and AstraZeneca. Institutional honoraria for participation in advisory boards or in Independent Data Monitoring Committees and Steering Committees from AAA International, Amgen, AstraZeneca, Astellas Pharma, Bayer, Bristol-Myers Squibb, DAIICHI Sankyo, Janssen, Modra Pharmaceuticals, MSD, Myriad Genetic, Novartis, Orion, Pfizer, Roche, Telixpharma, Tolermo Pharmaceutcials; invited speaker for Swiss group for Clinical Cancer Research (SAKK), Cold Spring Harbor Laboratory, ASCO GU; other honoraria from PeerVoice, Silvio Grasso Consulting, WebMD-Medscape. Patent royalties and other intellectual property for a research method for biomarker WO2009138392 Ursula Vogl: Advisory role (institutional): Janssen, Astellas, Merck, MSD, Pfizer, Roche, Bayer, BMS, Novartis AAA. Travel support: Janssen, Merck, Ipsen; Speakers Bureau (compensated, institutional): Janssen, Astellas, Pfizer, Roche, SAMO, BMS, Ipsen. Grant: Fond'Action The remaining authors declare no conflict of interest., (Copyright © 2024 Elsevier Inc. All rights reserved.)
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- 2024
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114. Activity of Lutetium-177 Prostate-specific Membrane Antigen and Determinants of Outcomes in Patients with Metastatic Castration-resistant Prostate Cancer Previously Treated with Cabazitaxel: The PACAP Study.
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Flippot R, Telli T, Velev M, Fléchon A, De Vries-Brilland M, Turpin L, Bergman A, Turco F, Mahammedi H, Fendler WP, Giraudet AL, Josset Q, Montravers F, Vogel W, Gillessen S, Berardi Vilei S, Herrmann K, Kryza D, Paone G, Hadaschik B, Merlin C, Dufour PA, Bernard-Tessier A, Naoun N, Patrikidou A, Garcia C, Foulon S, Pagès A, and Fizazi K
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- Humans, Male, Aged, Retrospective Studies, Middle Aged, Treatment Outcome, Aged, 80 and over, Glutamate Carboxypeptidase II metabolism, Antigens, Surface metabolism, Progression-Free Survival, Neoplasm Metastasis, Prostatic Neoplasms, Castration-Resistant drug therapy, Prostatic Neoplasms, Castration-Resistant pathology, Lutetium therapeutic use, Taxoids therapeutic use, Radioisotopes therapeutic use, Prostate-Specific Antigen blood
- Abstract
Background: Both cabazitaxel and lutetium-177 prostate-specific membrane antigen (Lu-PSMA) improve survival in metastatic castration-resistant prostate cancer (mCRPC) after an androgen receptor pathway inhibitor and docetaxel, but there are limited data regarding Lu-PSMA activity after cabazitaxel., Objective: To assess the activity of Lu-PSMA and determinants of outcomes after cabazitaxel in mCRPC., Design, Setting, and Participants: A retrospective analysis was conducted of consecutive mCRPC patients from eight European centers treated with Lu-PSMA after cabazitaxel., Intervention: Lu-PSMA every 6-8 wk at a dose of 6-7.6 GBq., Outcome Measurements and Statistical Analysis: The primary endpoint was radiographic progression-free survival (rPFS). The secondary endpoints included time to prostate-specific antigen (PSA) progression (TTPSA), overall survival (OS), PSA decline, objective response rate (ORR), clinical benefit, and safety., Results and Limitations: Of 126 patients, 68% had International Society of Urological Pathology (ISUP) grade 4-5 disease, 21% had visceral metastases, and 7% had lymph node disease only. DNA damage repair (DDR) alterations were detected in 11/50 (22%) patients with available testing. Patients received a median number of 3 Lu-PSMA cycles (interquartile range 2-4). With a median follow-up of 12.0 mo, the median rPFS was 4.4 mo (95% confidence interval [CI] 3.2-5.4), TTPSA 3.5 mo (95% CI 3.0-4.6), and OS 8.9 mo (95% CI 6.5-12.7). The ORR was 35%, and 55 patients (44%) experienced a PSA decline of ≥50%. The time to castration resistance of <12 mo was associated with shorter rPFS (p = 0.01). A similar trend was observed for ISUP grade 4-5 (p = 0.08), and baseline positron-emission tomography parameters including PSMA mean standardized uptake value (SUV) and maximum SUV (respectively, p = 0.06 and 0.05). The duration of previous cabazitaxel or DDR status did not impact outcomes. Patients experiencing a PSA decline of ≥ 50% on therapy demonstrated longer rPFS, TTPSA, and OS (all p < 0.0001). Limitations include retrospective data collection and investigator-based rPFS assessment., Conclusions: Lu-PSMA demonstrated a substantial PSA decline but limited rPFS after cabazitaxel in a real-life setting. Adverse baseline characteristics, baseline positron-emission tomography parameters, and quality of PSA response may help identify patients less likely to benefit from Lu-PSMA., Patient Summary: Lutetium-177 prostate-specific membrane antigen (Lu-PSMA) improved outcomes in patients with castration-resistant prostate cancer, but there are limited data about its activity after cabazitaxel, a chemotherapy that is also the standard of care in this setting. We conducted a study across eight European centers and showed substantial responses on Lu-PSMA after cabazitaxel, although activity was short lived in a heavily pretreated population. Our findings prompt for real-life evaluation of Lu-PSMA in earlier settings to define the best therapeutic sequence., (Copyright © 2024 European Association of Urology. Published by Elsevier B.V. All rights reserved.)
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- 2024
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115. Safety profile of darolutamide versus placebo: a systematic review and meta-analysis.
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Turco F, Gillessen S, Treglia G, Fizazi K, Smith MR, Tombal B, Cathomas R, Buttigliero C, Di Maio M, Tucci M, and Vogl UM
- Subjects
- Humans, Male, Pyrazoles adverse effects, Pyrazoles therapeutic use, Androgen Receptor Antagonists therapeutic use, Androgen Receptor Antagonists adverse effects, Prostatic Neoplasms drug therapy, Prostatic Neoplasms pathology
- Abstract
Background: Darolutamide is an androgen receptor pathway inhibitor (ARPI) used in patients with prostate cancer (PC). In pivotal trials, it has demonstrated a favorable toxicity profile. There are no head-to-head comparison studies between the different ARPIs, but the efficacy of these drugs seems to be similar making the toxicity profile a key element for treatment selection., Methods: We conducted a systematic review of all clinical trials assessing treatment with darolutamide for patients with PC using placebo as the control using the PubMed/Medline and Cochrane library databases. We also performed a meta-analysis to compare the safety of darolutamide versus placebo evaluating adverse events (AE) leading to treatment discontinuation and the rate of the AE reported as "AE of interest" in the ARAMIS trial. The comparison among darolutamide and the placebo group in terms of safety and tolerability was performed using odds ratio (OR) as meta-analytic outcome., Results: We identified three articles comprising 2902 patients for the systematic review and meta-analysis (1652 treated with darolutamide and 1250 with placebo). Darolutamide did not increase AE leading to treatment discontinuation compared to placebo (pooled OR: 1.176, 95% CI 0.918-1.507, p = 0.633). Regarding the "AE of interest" there was no difference between darolutamide and placebo in terms of asthenia, cardiac arrhythmia, cardiac disorder, coronary artery disorder, depression mood disorder, falls, fatigue, heart failure, hot flushes, hypertension, mental-impairment disorder, rash, seizure and weight loss. The only "AE of interest" with a statistically significant difference in favor of placebo was bone fractures (pooled OR: 1.523, 95% CI 1.081-2.146)., Conclusions: In our systematic review and meta-analysis, darolutamide showed a toxicity profile comparable to placebo with the exception of bone fractures. In the absence of head-to-head comparison studies between the different ARPIs, the results of our research suggest a preferred use of darolutamide in the approved settings., (© 2023. The Author(s), under exclusive licence to Springer Nature Limited.)
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- 2024
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116. Is There a Place for De-escalating Therapy in Patients with Metastatic Hormone-sensitive Prostate Cancer?
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Turco F, Tombal B, Gillessen S, and Omlin A
- Abstract
Although intermittent androgen deprivation therapy was often recommended for metastatic hormone-sensitive cancer therapy in the past, we do not know whether its use can be extrapolated to combination therapy. Trials evaluating intermittent therapy are necessary as this strategy could improve patient quality of life and reduce adverse events and costs., (Copyright © 2024 European Association of Urology. Published by Elsevier B.V. All rights reserved.)
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- 2024
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117. Treatment options in first-line metastatic renal carcinoma: A meta-analysis of 2556 patients treated with immune checkpoint inhibitors-based combinations in randomised controlled trials.
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Tucci M, Mandarà M, Giuliani J, Durante E, Buttigliero C, Turco F, Palesandro E, Campisi I, Singh N, Muraro M, Munoz F, and Fiorica F
- Subjects
- Humans, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Randomized Controlled Trials as Topic, Sunitinib therapeutic use, Carcinoma, Renal Cell drug therapy, Immune Checkpoint Inhibitors therapeutic use, Kidney Neoplasms drug therapy, Kidney Neoplasms pathology
- Abstract
Background & Aims: The average five-year survival of metastatic renal cell carcinoma (mRCC) is 71%. However, there is significant variability in patient prognosis. Immune checkpoint inhibitors (ICIs) have been introduced into the treatment landscape of mRCC. This meta-analysis aimed to estimate progression-free and overall survival probabilities and identify possible outcome predictors of mRCC patients treated with ICI combination as first-line treatment., Methods: Studies comparing the combination of ICI combinations versus standard of therapy for first-line treatment of advanced renal-cell carcinoma were searched in MEDLINE, CANCERLIT, the Cochrane Controlled Trials Register, and the Cochrane Library from inception through September 2023. Data on patient populations and outcomes were extracted from each study by three independent observers and combined using the DerSimonian and Laird methods., Results: Six studies met the inclusion criteria. Globally, 5121 patients were included in this meta-analysis: 2556 patients treated with immune checkpoint inhibitors and 2565 with sunitinib as control. The ICI combination was associated with improved PFS (hazard ratio (HR) 0.68; 95 % confidence interval (CI), 0.56-0.81, p < 0.0001). Furthermore, ICI combination was also associated with OS improvement (HR 0.85; 95 % CI, 0.78-0.92, p = 0.001). There is no statistical increase in adverse events., Conclusions: Our findings show that PFS and OS are statistically increased in mRCC with ICI combination treatment by 32% and 15%, respectively., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)
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- 2024
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118. TEAM Study: Upfront Docetaxel Treatment in Patients With Metastatic Hormone-Sensitive Prostate Cancer: A Real-World, Multicenter, Retrospective Analysis.
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Pisano C, Turco F, Arnaudo E, Fea E, Vanella P, Ruatta F, Filippi R, Brusa F, Prati V, Vana F, Mennitto A, Cattrini C, Vignani F, Dionisio R, Icardi M, Guglielmini P, Buosi R, Stevani I, Vormola R, Numico G, Depetris I, Comandone A, Gennari A, Airoldi M, Rossi M, Vellani G, Ortega C, Tucci M, Maio MD, and Buttigliero C
- Subjects
- Male, Humans, Docetaxel, Retrospective Studies, Analgesics, Opioid therapeutic use, Androgen Antagonists therapeutic use, Treatment Outcome, Antineoplastic Combined Chemotherapy Protocols, Pain etiology, Hormones, Prostate-Specific Antigen, Prostatic Neoplasms pathology
- Abstract
Background: Treatment of metastatic hormone-sensitive prostate cancer (mHSPC) dramatically changed. PEACE-1 and ARASENS trials established triplet therapy efficacy. Identifying prognostic factors supporting treatment choice is pivotal., Methods: TEAM is an observational, retrospective study to evaluate prognostic role of variables in mHSPC patients receiving upfront docetaxel in 11 Italian centers. Outcome measures were progression-free survival (PFS) and overall-survival (OS)., Results: From September 2014 to December 2020, 147 patients were included. Median PFS and OS were 11.6 and 37.4 months. At univariate analysis, PFS-related variables were Gleason Score (GS) (P = .001), opioid use (P = .004), bone metastases number (P < .001), baseline PSA (P = .006), Hb (P < .001), ALP (P < .001) and LDH (P = .002), time between ADT and docetaxel start (P = .018), 3-month PSA (P < .001) and ALP (P < .001), and number of docetaxel cycles (P < .001). OS-related variables were PSA at diagnosis (P = .024), primary tumor treatment (P = .022), baseline pain (P = .015), opioid use (P < .001), bone metastases number (P < . 001), baseline Hb (P < .001), ALP (P < .001) and LDH (P = .001), NLR ratio (P = .039), 3-month PSA (P < .001) and ALP (P < .001) and docetaxel cycles number (P < .001). At multivariate analysis, independent prognostic variables were GS, opioid use, baseline LDH and time between ADT and docetaxel initiation for PFS, and baseline Hb and LDH for OS., Conclusion: Patients receiving upfront docetaxel with high GS, high disease burden, pain or opioid use, baseline unfavorable laboratory values had worse outcomes. Patients had greater docetaxel benefit when initiated early after ADT start. These parameters could be taken into account when selecting candidates for triplet therapy., Competing Interests: Disclosure All authors have no conflict of interest to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)
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- 2024
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119. Darolutamide in Metastatic Prostate Cancer.
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Turco F, Tucci M, and Buttigliero C
- Subjects
- Hormones, Humans, Male, Pyrazoles adverse effects, Androgen Receptor Antagonists, Prostatic Neoplasms drug therapy
- Published
- 2022
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120. S100B protein in the gut: the evidence for enteroglial-sustained intestinal inflammation.
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Cirillo C, Sarnelli G, Esposito G, Turco F, Steardo L, and Cuomo R
- Subjects
- Animals, Astrocytes metabolism, Brain metabolism, Central Nervous System metabolism, Glial Fibrillary Acidic Protein metabolism, Humans, Immunosuppressive Agents therapeutic use, Intestinal Diseases metabolism, Nitric Oxide chemistry, S100 Calcium Binding Protein beta Subunit, Inflammation metabolism, Intestinal Mucosa metabolism, Microglia metabolism, Nerve Growth Factors biosynthesis, Neuroglia metabolism, S100 Proteins biosynthesis
- Abstract
Glial cells in the gut represent the morphological and functional equivalent of astrocytes and microglia in the central nervous system (CNS). In recent years, the role of enteric glial cells (EGCs) has extended from that of simple nutritive support for enteric neurons to that of being pivotal participants in the regulation of inflammatory events in the gut. Similar to the CNS astrocytes, the EGCs physiologically express the S100B protein that exerts either trophic or toxic effects depending on its concentration in the extracellular milieu. In the CNS, S100B overexpression is responsible for the initiation of a gliotic reaction by the release of pro-inflammatory mediators, which may have a deleterious effect on neighboring cells. S100B-mediated pro-inflammatory effects are not limited to the brain: S100B overexpression is associated with the onset and maintenance of inflammation in the human gut too. In this review we describe the major features of EGCs and S100B protein occurring in intestinal inflammation deriving from such.
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- 2011
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