Intestinal Barrier Dysfunction and Microbial Translocation in Patients with First-Diagnosed Atrial Fibrillation.
LPS
atrial fibrillation
biomarkers
endotoxaemia
endotoxin
fibrosis
gut-heart axis
heart failure
leaky gut
microbial translocation
Journal
Biomedicines
ISSN: 2227-9059
Titre abrégé: Biomedicines
Pays: Switzerland
ID NLM: 101691304
Informations de publication
Date de publication:
10 Jan 2023
10 Jan 2023
Historique:
received:
13
12
2022
revised:
03
01
2023
accepted:
06
01
2023
entrez:
21
1
2023
pubmed:
22
1
2023
medline:
22
1
2023
Statut:
epublish
Résumé
According to the leaky gut concept, microbial products (e.g., lipopolysaccharide, LPS) enter the circulation and mediate pro-inflammatory immunological responses. Higher plasma LPS levels have been reported in patients with various cardiovascular diseases, but not specifically during early atrial fibrillation (AF). We studied data and blood samples from patients presenting with first-diagnosed AF (FDAF) ( Circulating biomarkers that are suggestive of mucosal inflammation (zonulin, mucosal adhesion molecule MAdCAM-1) and intestinal epithelium damage (intestinal fatty acid binding protein, IFABP) were increased in the plasma of patients with FDAF when compared to patients with chronic cardiovascular diseases but without AF. Surrogate plasma markers of increased intestinal permeability (LPS, CD14, LPS-binding protein, gut-derived LPS-neutralising IgA antibodies, EndoCAbs) were detected during early AF. A reduced ratio of IgG/IgM EndoCAbs titres indicated chronic endotoxaemia. Collagen turnover biomarkers, which corresponded to the LPS values, suggested an association of gut-derived low-grade endotoxaemia with adverse structural remodelling. The LPS concentrations were higher in FDAF patients who experienced a major adverse cardiovascular event. Intestinal barrier dysfunction and microbial translocation accompany FDAF. Improving gut permeability and low-grade endotoxaemia might be a potential therapeutic approach to reducing the disease progression and cardiovascular complications in FDAF.
Sections du résumé
BACKGROUND
BACKGROUND
According to the leaky gut concept, microbial products (e.g., lipopolysaccharide, LPS) enter the circulation and mediate pro-inflammatory immunological responses. Higher plasma LPS levels have been reported in patients with various cardiovascular diseases, but not specifically during early atrial fibrillation (AF).
METHODS
METHODS
We studied data and blood samples from patients presenting with first-diagnosed AF (FDAF) (
RESULTS
RESULTS
Circulating biomarkers that are suggestive of mucosal inflammation (zonulin, mucosal adhesion molecule MAdCAM-1) and intestinal epithelium damage (intestinal fatty acid binding protein, IFABP) were increased in the plasma of patients with FDAF when compared to patients with chronic cardiovascular diseases but without AF. Surrogate plasma markers of increased intestinal permeability (LPS, CD14, LPS-binding protein, gut-derived LPS-neutralising IgA antibodies, EndoCAbs) were detected during early AF. A reduced ratio of IgG/IgM EndoCAbs titres indicated chronic endotoxaemia. Collagen turnover biomarkers, which corresponded to the LPS values, suggested an association of gut-derived low-grade endotoxaemia with adverse structural remodelling. The LPS concentrations were higher in FDAF patients who experienced a major adverse cardiovascular event.
CONCLUSIONS
CONCLUSIONS
Intestinal barrier dysfunction and microbial translocation accompany FDAF. Improving gut permeability and low-grade endotoxaemia might be a potential therapeutic approach to reducing the disease progression and cardiovascular complications in FDAF.
Identifiants
pubmed: 36672684
pii: biomedicines11010176
doi: 10.3390/biomedicines11010176
pmc: PMC9856173
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : German Cardiac Society
ID : DGK03/2021
Organisme : German Heart Research Foundation
ID : F/14/20
Organisme : Berlin Institute of Health at Charité - Universitätsmedizin Berlin
ID : Clinician Scientist Program
Organisme : Deutsche Forschungsgemeinschaft
ID : WI 5229/1-1
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