Adipose tissue derived bacteria are associated with inflammation in obesity and type 2 diabetes.
Adipose Tissue
/ immunology
Bacterial Translocation
/ immunology
Cells, Cultured
DNA, Bacterial
/ isolation & purification
Diabetes Mellitus, Type 2
/ complications
Female
Firmicutes
/ isolation & purification
Humans
Inflammation
/ immunology
Interleukin-6
/ metabolism
Intestinal Mucosa
/ metabolism
Male
Middle Aged
Obesity
/ complications
Proteobacteria
/ isolation & purification
RNA, Ribosomal, 16S
/ blood
Tumor Necrosis Factor-alpha
/ metabolism
bacterial translocation
inflammation
intestinal permeability
obesity
obesity surgery
Journal
Gut
ISSN: 1468-3288
Titre abrégé: Gut
Pays: England
ID NLM: 2985108R
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
18
10
2019
revised:
31
03
2020
accepted:
31
03
2020
pubmed:
23
4
2020
medline:
10
4
2021
entrez:
23
4
2020
Statut:
ppublish
Résumé
Bacterial translocation to various organs including human adipose tissue (AT) due to increased intestinal permeability remains poorly understood. We hypothesised that: (1) bacterial presence is highly tissue specific and (2) related in composition and quantity to immune inflammatory and metabolic burden. We quantified and sequenced the bacterial 16S rRNA gene in blood and AT samples (omental, mesenteric and subcutaneous) of 75 subjects with obesity with or without type 2 diabetes (T2D) and used catalysed reporter deposition (CARD) - fluorescence in situ hybridisation (FISH) to detect bacteria in AT. Under stringent experimental and bioinformatic control for contaminants, bacterial DNA was detected in blood and omental, subcutaneous and mesenteric AT samples in the range of 0.1 to 5 pg/µg DNA isolate. Moreover, CARD-FISH allowed the detection of living, AT-borne bacteria. Our study provides contaminant aware evidence for the presence of bacteria and bacterial DNA in several ATs in obesity and T2D and suggests an important role of bacteria in initiating and sustaining local AT subclinical inflammation and therefore impacting metabolic sequelae of obesity.
Identifiants
pubmed: 32317332
pii: gutjnl-2019-320118
doi: 10.1136/gutjnl-2019-320118
doi:
Substances chimiques
DNA, Bacterial
0
IL6 protein, human
0
Interleukin-6
0
RNA, Ribosomal, 16S
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1796-1806Commentaires et corrections
Type : CommentIn
Informations de copyright
© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: None declared.