2026-07-21T20:00:01Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/180872024-11-28T14:43:09Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927

00925njm 22002777a 4500 dc Serena, Carolina author Queipo-Ortuño, Maribel author Millan, Monica author Sanchez-Alcoholado, Lidia author Caro, Aleidis author Espina, Beatriz author Menacho, Margarita author Bautista, Michelle author Monfort-Ferré, Diandra author Terrón-Puig, Margarida author Núñez-Roa, Catalina author Maymó-Masip, Elsa author Rodriguez, M. Mar author Tinahones, Francisco J. author Espin, Eloy author Martí, Marc author Fernández-Veledo, Sonia author Vendrell, Joan author 2020-07-31 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. 10.3390/jcm9082448 2077-0383 Journal of Clinical Medicine http://hdl.handle.net/10668/3865 32751800 http://hdl.handle.net/20.500.12105/18087 Tissue microbiota Inflammatory bowel disease 16S sequencing Creeping fat PICRUSt analysis Escherichia coli Fusobacterium Lipopolysaccharide biosynthesis Microbiota Enfermedad inflamatoria intestinal ARN ribosómico 16S Lipopolisacáridos Tejidos Enfermedad de Crohn Tejido adiposo Microbial Signature in Adipose Tissue of Crohn's Disease Patients