RT Journal Article
T1 Microbial Signature in Adipose Tissue of Crohn's Disease Patients.
A1 Serena, Carolina
A1 Queipo-Ortuño, Maribel
A1 Millan, Monica
A1 Sanchez-Alcoholado, Lidia
A1 Caro, Aleidis
A1 Espina, Beatriz
A1 Menacho, Margarita
A1 Bautista, Michelle
A1 Monfort-Ferré, Diandra
A1 Terrón-Puig, Margarida
A1 Núñez-Roa, Catalina
A1 Maymó-Masip, Elsa
A1 Rodriguez, M Mar
A1 Tinahones, Francisco J
A1 Espin, Eloy
A1 Martí, Marc
A1 Fernández-Veledo, Sonia
A1 Vendrell, Joan
K1 16S sequencing
K1 Escherichia coli
K1 Fusobacterium
K1 PICRUSt analysis
K1 creeping fat
K1 inflammatory bowel disease
K1 lipopolysaccharide biosynthesis
K1 tissue microbiota
AB 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.
SN 2077-0383
YR 2020
FD 2020-07-31
LK https://hdl.handle.net/10668/26845
UL https://hdl.handle.net/10668/26845
LA en
DS RISalud
RD Apr 19, 2025