Browsing by Keyword "Enfermedad de Crohn"
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Publication Gene Signatures of Early Response to Anti-TNF Drugs in Pediatric Inflammatory Bowel Disease(Multidisciplinary Digital Publishing Institute (MDPI), 2020-05-09) Salvador-Martín, Sara; Raposo-Gutiérrez, Irene; Navas-López, Víctor Manuel; Gallego-Fernández, Carmen; Moreno-Álvarez, Ana; Solar-Boga, Alfonso; Muñoz-Codoceo, Rosana; Magallares, Lorena; Martínez-Ojinaga, Eva; Fobelo, María J.; Millán-Jiménez, Antonio; Rodriguez-Martinez, Alejandro; Vayo, Concepción A.; Sánchez, Cesar; Tolin, Mar; Bossacoma, Ferrán; Pujol-Muncunill, Gemma; González de Caldas, Rafael; Loverdos, Inés; Blanca-García, José A.; Segarra, Oscar; Eizaguirre, Francisco J.; García-Romero, Ruth; Merino-Bohórquez, Vicente; Sanjurjo-Sáez, María; López-Fernández, Luis A.; [Salvador-Martín,S; Raposo-Gutiérrez,I; Sanjurjo-Sáez,M; López-Fernández,LA] Pharmacy Department, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain. [Navas-López,V] Pediatric Gastroenterology and Nutrition Unit, Hospital Regional Universitario de Málaga, IBIMA Multidisciplinary Group for Pediatric Research, Málaga, Spain. [Gallego-Fernández,C] Pharmacy Department, Hospital Regional Universitario de Málaga, Málaga, Spain. [Moreno-Álvarez,A; Solar-Boga,A] Pediatric Gastroenterology Unit, Department of Pediatrics, A Coruña University Hospital, A Coruña, Spain. [Muñoz-Codoceo,R] Department of Pediatric Gastroenterology, Hospital Infantil Universitario Niño Jesús, Madrid, Spain. [Magallares,L; Martínez-Ojinaga,E] Department of Pediatric Gastroenterology, University Hospital La Paz, Madrid, Spain. [Fobelo,MJ] Pharmacy Service, Hospital Virgen de Valme, Sevilla, Spain. [Millán-Jiménez,A] Pediatric Gastroenterology Unit, Hospital Virgen de Valme, Sevilla, Spain. [Rodriguez-Martinez,A] Pediatric Gastroenterology, Hepatology and Nutrition Unit, Hospital Universitario Virgen del Rocio, Seville, Spain. [Vayo,CA] Pharmacy Service, Hospital Universitario Virgen del Rocio, Seville, Spain. [Sánchez,C; Tolin,M] Gastroenterology Unit, Hospital General Universitario Gregorio Marañón, Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain. [Bossacoma,F] Fundació Sant Joan de Déu, Fundació Salut Emporda, Barcelona, Spain. [Pujol-Muncunill;G] Department of Pediatric Gastroenterology, Hepatology and Nutrition, Hospital Sant Joan de Déu, Barcelona, Spain. [González de Caldas,R] Pediatric Gastroenterology Unit, Hospital Reina Sofía, Córdoba, Spain. [Loverdos,I] Pediatric Gastroenterology, Hepatology and Nutrition Unit, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Barcelona, Spain. [Blanca-García,JA] Pediatric Gastroenterology Unit, Hospital Puerta del Mar, Cadiz, Spain. [Segarra,O] Pediatric Gastroenterology Unit, Hospital Universitario Vall d’Hebrón, Barcelona, Spain. [Eizaguirre,FJ] Pediatric Gastroenterology Unit, Hospital Universitario Donostia, San Sebastián, Spain. [García-Romero,R] Pediatric Gastroenterology Unit, Hospital Infantil Miguel Servet, Zaragoza, Spain. [Merino-Bohórquez,V] UGC Pharmacy Department, Hospital Virgen de la Macarena, Sevilla, Spain.Around a 20-30% of inflammatory bowel disease (IBD) patients are diagnosed before they are 18 years old. Anti-TNF drugs can induce and maintain remission in IBD, however, up to 30% of patients do not respond. The aim of the work was to identify markers that would predict an early response to anti-TNF drugs in pediatric patients with IBD. The study population included 43 patients aged <18 years with IBD who started treatment with infliximab or adalimumab. Patients were classified into primary responders (n = 27) and non-responders to anti-TNF therapy (n = 6). Response to treatment could not be analyzed in 10 patients. Response was defined as a decrease in over 15 points in the disease activity indexes from week 0 to week 10 of infliximab treatment or from week 0 to week 26 of adalimumab treatment. The expression profiles of nine genes in total RNA isolated from the whole-blood of pediatric IBD patients taken before biologic administration and after 2 weeks were analyzed using qPCR and the 2-∆∆Ct method. Before initiation and after 2 weeks of treatment the expression of SMAD7 was decreased in patients who were considered as non-responders (p value < 0.05). Changes in expression were also observed for TLR2 at T0 and T2, although that did not reach the level of statistical significance. In addition, the expression of DEFA5 decreased 1.75-fold during the first 2 weeks of anti-TNF treatment in responders, whereas no changes were observed in non-responders. Expression of the SMAD7 gene is a pharmacogenomic biomarker of early response to anti-TNF agents in pediatric IBD. TLR2 and DEFA5 need to be validated in larger studies.Publication Microbial Signature in Adipose Tissue of Crohn's Disease Patients(Multidisciplinary Digital Publishing Institute (MDPI), 2020-07-31) Serena, Carolina; Queipo-Ortuño, Maribel; Millan, Monica; Sanchez-Alcoholado, Lidia; Caro, Aleidis; Espina, Beatriz; Menacho, Margarita; Bautista, Michelle; Monfort-Ferré, Diandra; Terrón-Puig, Margarida; Núñez-Roa, Catalina; Maymó-Masip, Elsa; Rodriguez, M. Mar; Tinahones, Francisco J.; Espin, Eloy; Martí, Marc; Fernández-Veledo, Sonia; Vendrell, Joan; [Serena,C; Monfort-Ferré,D; Terrón-Puig,M; Núñez-Roa,C; Maymó-Masip,E; Rodriguez,MM; Fernández-Veledo,S; Vendrell,J] Hospital Universitari de Tarragona Joan XXIII, Institut d’Investigació Sanitària Pere Virgili Universitat Rovira i Virgili, Tarragona, Spain. [Serena,C; Terrón-Puig,M; Núñez-Roa,C; Maymó-Masip,E; Rodriguez,MM; Fernández-Veledo,S; Vendrell,J] CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Madrid, Spain. [Queipo-Ortuño,M; Sanchez-Alcoholado,L] CIBER de Obesidad y Nutrición (CIBERObN), Instituto de Salud Carlos III, Madrid, Spain. [Queipo-Ortuño,M; Sanchez-Alcoholado,L] Unidad de Gestión Clínica Intercentros de Oncología Medica, Hospitales Universitarios Regional y Virgen de la Victoria de Málaga, Instituto de Investigación Biomédica de Málaga (IBIMA)-CIMES-UMA, Málaga, Spain. [Millan,M; Caro,A; Espina,B] Colorectal Surgery Unit, Hospital Universitari Joan XXIII, Tarragona, Spain. [Millan,M] Colorectal Surgery Unit, Hospital Universitari La Fe, Valencia, Spain. [Menacho,M; Bautista,M] Digestive Unit, University Hospital Joan XXIII, IISPV, Tarragona, Spain. [Tinahones,FJ] Endocrinology and Nutrition Department, Biomedical Research Institute from Malaga (IBIMA), University Hospital Virgen de la Victoria of Malaga, Malaga University, Málaga, Spain. [Espin,E; Martí,M] Colorectal Surgery Unit, General Surgery Service, Valle Hebron Hospital, Autonomous University of Barcelona, Barcelona, Spain. [Vendrell,J] Medicine and Surgery Department, School of Medicine, Universitat Rovira i Virgili, Tarragona, Spain.Crohn's disease (CD) is characterized by compromised immune tolerance to the intestinal commensal microbiota, intestinal barrier inflammation, and hyperplasia of creeping fat (CF) and mesenteric adipose tissue (AT), which seems to be directly related to disease activity. Gut microbiota dysbiosis might be a determining factor in CD etiology, manifesting as a low microbial diversity and a high abundance of potentially pathogenic bacteria. We tested the hypothesis that CF is a reservoir of bacteria through 16S-rRNA sequencing of several AT depots of patients with active and inactive disease and controls. We found a microbiome signature within CF and mesenteric AT from patients, but not in subcutaneous fat. We failed to detect bacterial DNA in any fat depot of controls. Proteobacteria was the most abundant phylum in both CF and mesenteric AT, and positively correlated with fecal calprotectin/C-reactive protein. Notably, the clinical status of patients seemed to be related to the microbiome signature, as those with the inactive disease showed a reduction in the abundance of pathogenic bacteria. Predictive functional profiling revealed many metabolic pathways including lipopolysaccharide biosynthesis and sulfur metabolism overrepresented in active CD relative to that in inactive CD. Our findings demonstrate that microbiota dysbiosis associated with CD pathophysiology is reflected in AT and might contribute to disease severity.Publication Peroxisome Proliferator-Activated Receptors: Experimental Targeting for the Treatment of Inflammatory Bowel Diseases(Frontiers Media, 2020-05-27) Decara, Juan; Rivera, Patricia; López-Gambero, Antonio Jesús; Serrano, Antonia; Pavón, Francisco-Javier; Baixeras, Elena; Rodríguez de Fonseca, Fernando; Suárez, Juan; [Decara,J; López-Gambero,AJ; Serrano,A; Pavón, Francisco-Javier; Rodríguez de Fonseca,F; Suárez,J] UGC Salud Mental, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Regional Universitario de Málaga, Universidad de Málaga, Málaga, Spain. [Rivera,P] Departamento de Endocrinología, Fundación Investigación Biomédica del Hospital Infantil Universitario Niño Jesús, Madrid, Spain. [Pavón,FJ] Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV) and UGC del Corazón, Instituto de Investigación Biomédica de Málaga (IBIMA), Hospital Universitario Virgen de la Victoria, Universidad de Málaga, Málaga, Spain. [Baixeras,E] Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Universidad de Málaga, IBIMA, Málaga, Spain.The peroxisome proliferator-activated receptors (PPARs) are a group of nuclear receptor proteins that promote ligand-dependent transcription of target genes that regulate energy production, lipid metabolism, and inflammation. The PPAR superfamily comprises three subtypes, PPARα, PPARγ, and PPARβ/δ, with differential tissue distributions. In addition to their different roles in the regulation of energy balance and carbohydrate and lipid metabolism, an emerging function of PPARs includes normal homeostasis of intestinal tissue. PPARα activation represses NF-κB signaling, which decreases the inflammatory cytokine production by different cell types, while PPARγ ligands can inhibit activation of macrophages and the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin (IL)-6, and Il-1β. In this regard, the anti-inflammatory responses induced by PPAR activation might restore physiopathological imbalances associated with inflammatory bowel diseases (IBD). Thus, PPARs and their ligands have important therapeutic potential. This review briefly discusses the roles of PPARs in the physiopathology and therapies of the most important IBDs, ulcerative colitis (UC), and Crohn's disease (CD), as well some new experimental compounds with PPAR activity as promising drugs for IBD treatment.