Intestinal fatty acid binding protein is associated with cardiac function and gut dysbiosis in chronic heart failure.
dysbiosis
gut leakage
gut microbiota
heart failure
intestinal fatty acid binding protein (I-FABP)
Journal
Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388
Informations de publication
Date de publication:
2023
2023
Historique:
received:
06
02
2023
accepted:
18
05
2023
medline:
19
6
2023
pubmed:
19
6
2023
entrez:
19
6
2023
Statut:
epublish
Résumé
The gut microbiota in patients with chronic heart failure (HF) is characterized by low bacterial diversity and reduced ability to synthesize beneficial metabolites. These changes may facilitate leakage of whole bacteria or bacterial products from the gut into the bloodstream, which may activate the innate immune system and contribute to the low-grade inflammation seen in HF. In this exploratory cross-sectional study, we aimed to investigate relationships between gut microbiota diversity, markers of gut barrier dysfunction, inflammatory markers, and cardiac function in chronic HF patients. In total, 151 adult patients with stable HF and left ventricular ejection fraction (LVEF) < 40% were enrolled. We measured lipopolysaccharide (LPS), LPS-binding protein (LBP), intestinal fatty acid binding protein (I-FABP), and soluble cluster of differentiation 14 (sCD14) as markers of gut barrier dysfunction. N-terminal pro-B-type natriuretic peptide (NT-proBNP) level above median was used as a marker of severe HF. LVEF was measured by 2D-echocardiography. Stool samples were sequenced using 16S ribosomal RNA gene amplification. Shannon diversity index was used as a measure of microbiota diversity. Patients with severe HF (NT-proBNP > 895 pg/ml) had increased I-FABP ( In patients with HF, I-FABP, a marker of enterocyte damage, is associated with HF severity and low microbial diversity as part of an altered gut microbiota composition. I-FABP may reflect dysbiosis and may be a marker of gut involvement in patients with HF.
Sections du résumé
Background
UNASSIGNED
The gut microbiota in patients with chronic heart failure (HF) is characterized by low bacterial diversity and reduced ability to synthesize beneficial metabolites. These changes may facilitate leakage of whole bacteria or bacterial products from the gut into the bloodstream, which may activate the innate immune system and contribute to the low-grade inflammation seen in HF. In this exploratory cross-sectional study, we aimed to investigate relationships between gut microbiota diversity, markers of gut barrier dysfunction, inflammatory markers, and cardiac function in chronic HF patients.
Methods
UNASSIGNED
In total, 151 adult patients with stable HF and left ventricular ejection fraction (LVEF) < 40% were enrolled. We measured lipopolysaccharide (LPS), LPS-binding protein (LBP), intestinal fatty acid binding protein (I-FABP), and soluble cluster of differentiation 14 (sCD14) as markers of gut barrier dysfunction. N-terminal pro-B-type natriuretic peptide (NT-proBNP) level above median was used as a marker of severe HF. LVEF was measured by 2D-echocardiography. Stool samples were sequenced using 16S ribosomal RNA gene amplification. Shannon diversity index was used as a measure of microbiota diversity.
Results
UNASSIGNED
Patients with severe HF (NT-proBNP > 895 pg/ml) had increased I-FABP (
Conclusions
UNASSIGNED
In patients with HF, I-FABP, a marker of enterocyte damage, is associated with HF severity and low microbial diversity as part of an altered gut microbiota composition. I-FABP may reflect dysbiosis and may be a marker of gut involvement in patients with HF.
Identifiants
pubmed: 37332580
doi: 10.3389/fcvm.2023.1160030
pmc: PMC10272617
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1160030Informations de copyright
© 2023 Nendl, Raju, Broch, Mayerhofer, Holm, Halvorsen, Lappegård, Moscavitch, Hov, Seljeflot, Trøseid and Awoyemi.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
Metabolites. 2021 Jul 29;11(8):
pubmed: 34436434
Atherosclerosis. 2019 Jul;286:53-59
pubmed: 31100620
J Am Coll Cardiol. 2013 Aug 6;62(6):485-95
pubmed: 23747781
Shock. 2019 Apr;51(4):410-415
pubmed: 29847500
Front Microbiol. 2017 Jun 23;8:1162
pubmed: 28690602
Curr Res Microb Sci. 2021 Jun 17;2:100043
pubmed: 34841334
EBioMedicine. 2021 Aug;70:103511
pubmed: 34329947
J Clin Invest. 1974 Aug;54(2):326-38
pubmed: 4211161
JACC Basic Transl Sci. 2022 Mar 30;7(7):730-742
pubmed: 35958686
Circ Res. 2021 May 14;128(10):1421-1434
pubmed: 33983838
Clin Biochem. 2017 Jun;50(9):491-495
pubmed: 28232029
Adv Exp Med Biol. 2020;1276:27-35
pubmed: 32705592
World J Gastroenterol. 2010 Nov 14;16(42):5272-9
pubmed: 21072889
Transl Res. 2021 Feb;228:109-125
pubmed: 32841736
J Am Coll Cardiol. 2018 Mar 13;71(10):1184-1186
pubmed: 29519360
Exp Mol Med. 2013 Dec 06;45:e66
pubmed: 24310172
Prog Lipid Res. 2022 Jul;87:101178
pubmed: 35780915
PLoS One. 2017 Jun 27;12(6):e0179586
pubmed: 28654658
J Immunol. 2016 Sep 15;197(6):2390-9
pubmed: 27534554
ESC Heart Fail. 2018 Oct;5(5):977-984
pubmed: 30088346
JACC Heart Fail. 2016 Mar;4(3):220-7
pubmed: 26682791
ESC Heart Fail. 2017 Aug;4(3):282-290
pubmed: 28772054
EBioMedicine. 2020 Feb;52:102649
pubmed: 32062353
J Intern Med. 2015 Jun;277(6):717-26
pubmed: 25382824
ISME J. 2019 Jun;13(6):1520-1534
pubmed: 30742017
PLoS One. 2014 Dec 26;9(12):e115242
pubmed: 25541714
Circulation. 2017 Mar 7;135(10):964-977
pubmed: 27927713
J Pharmacol Exp Ther. 2021 Apr;377(1):39-50
pubmed: 33414131
J Am Coll Cardiol. 2023 May 2;81(17):1729-1739
pubmed: 37100490
Lancet. 1999 May 29;353(9167):1838-42
pubmed: 10359409