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Nowotny, H.F.* ; Zheng, T.* ; Seiter, T.M.* ; Ju, J.* ; Schneider, H.* ; Kroiss, M.* ; Sarkis, A.L.* ; Sturm, L.* ; Britz, V.* ; Lechner, A. ; Potzel, A. ; Kunz, S.* ; Bidlingmaier, M.* ; Neuhaus, K.* ; Gottschlich, A.* ; Kobold, S. ; Reisch, N.* ; Schirmer, M.* ; Reincke, M.* ; Adolf, C.*

Sex-dependent modulation of T and NK cells and gut microbiome by low sodium diet in patients with primary aldosteronism.

Front. Immunol. 15:1428054 (2024)
Verlagsversion DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
BACKGROUND: High dietary sodium intake is a major cardiovascular risk factor and adversely affects blood pressure control. Patients with primary aldosteronism (PA) are at increased cardiovascular risk, even after medical treatment, and high dietary sodium intake is common in these patients. Here, we analyze the impact of a moderate dietary sodium restriction on microbiome composition and immunophenotype in patients with PA. METHODS: Prospective two-stage clinical trial including two subgroups: 15 treatment-naive PA patients compared to matched normotensive controls; and 31 PA patients on mineralocorticoid receptor antagonist treatment before and three months after sodium restriction. Patients underwent blood pressure measurements, laboratory tests, analysis of peripheral blood mononuclear cells via flow cytometry and microbiome analysis. RESULTS: We observed a higher percentage of Tregs in treatment-naive PA patients (p = 0.0303), while the abundance of Bacteroides uniformis was higher in PA patients compared to normotensive controls (p = 0.00027) and the abundance of Lactobacillus species however was higher in the subgroup of normotensive controls (p = 0.0290). Sodium restriction was accompanied by a decrease in pro-inflammatory Tc17 cells in male patients (p = 0.0081, females p = 0.3274). Bacteroides uniformis abundance was higher in female patients (0.01230, p = 0.0016) and decreased upon sodium restriction (0.002309, p = 0.0068). CONCLUSION: Dietary sodium restriction in patients with PA modulates the peripheral immune cell composition toward a less inflammatory phenotype. This suggests a potential mechanism by which sodium reduction modulates immune cell composition, leading to blood pressure reduction and positively impacting cardiovascular risk.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Tc17 ; Tregs (regulatory T Cells) ; Microbiome ; Primary Aldosteronism (pa) ; Sodium; Cardiovascular Risk; Essential-hypertension; Blood-pressure; Reduction; Induction; Mortality; Chloride
Sprache englisch
Veröffentlichungsjahr 2024
HGF-Berichtsjahr 2024
ISSN (print) / ISBN 1664-3224
e-ISSN 1664-3224
Zeitschrift Frontiers in Immunology
Quellenangaben Band: 15, Heft: , Seiten: , Artikelnummer: 1428054 Supplement: ,
Verlag Frontiers
Verlagsort Avenue Du Tribunal Federal 34, Lausanne, Ch-1015, Switzerland
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Experimental Genetics (IEG)
Unit for Clinical Pharmacology (KKG-EKLiP)
POF Topic(s) 30201 - Metabolic Health
30203 - Molecular Targets and Therapies
Forschungsfeld(er) Genetics and Epidemiology
Immune Response and Infection
PSP-Element(e) G-521500-002
G-522100-001
Förderungen Bavarian Research Foundation
Deutsche Forschungsgemeinschaft (DFG)
TANGO
Bavarian Cancer Research Center (BZKF)
Frderprogramm fr Forschung und Lehre (FFoLe)
Eva Luise und Horst Khler Stiftung Else Krner-Fresenius-Stiftung
European Research Council (ERC) under the European Union
Else Krner-Fresenius Stiftung
international doctoral program 'i-Target: immunotargeting of cancer' - Elite Network of Bavaria
Hector Foundation
Fritz-Bender Foundation
European Research Council
Bundesministerium fr Bildung und Forschung
Bavarian Ministry for Economical Affairs
Institutional Strategy LMUexcellent of LMU Munich
Ernst Jung Stiftung
Wilhelm-Sander-Stiftung
German Cancer Aid
Else Kroner-Fresenius-Stiftung
Marie Sklodowska-Curie Training Network for Optimizing Adoptive T Cell Therapy of Cancer - Horizon 2020 programme of the European Union
Horizon 2020 programme of the European Union
Melanoma Research Alliance
Deutsche Forschungsgemeinschaft
DOI 10.3389/fimmu.2024.1428054
WOS ID 001387301700001
Scopus ID 85214012461
PubMed ID 39749333
Erfassungsdatum 2025-01-10
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