Evidence map›Paper›PMID 25497276›Full record

ArticleTranslational research : the journal of laboratory and clinical medicine2015

Effects of dietary salt levels on monocytic cells and immune responses in healthy human subjects: a longitudinal study.

Buqing Yi, Jens Titze, Marina Rykova, Matthias Feuerecker, Galina Vassilieva, Igor Nichiporuk, Gustav Schelling, Boris Morukov, Alexander Choukèr

Open access · greenAbstract read
In one paragraph

Article in Translational research : the journal of laboratory and clinical medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 2 pooled it
8.9field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 162 citations in OpenAlex.

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  15. Trained Innate Immunity in Animal Models of Cardiovascular Diseases.International journal of molecular sciences · 2024
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32 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Buqing YiHospital of the University of Munich (LMU), Department of Anaesthesiology, Munich, Germany.
Jens TitzeInterdisciplinary Center for Clinical Research, Friedrich-Alexander-University, Erlangen, Germany; Department of Nephrology and Hypertension, Friedrich-Alexander-University, Erlangen, Germany; Division of Clinical Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Marina RykovaInstitute for Biomedical Problems, Moscow, Russian Federation.
Matthias FeuereckerHospital of the University of Munich (LMU), Department of Anaesthesiology, Munich, Germany.
Galina VassilievaInstitute for Biomedical Problems, Moscow, Russian Federation.
Igor NichiporukInstitute for Biomedical Problems, Moscow, Russian Federation.
Gustav SchellingHospital of the University of Munich (LMU), Department of Anaesthesiology, Munich, Germany.
Boris MorukovInstitute for Biomedical Problems, Moscow, Russian Federation.
Alexander ChoukèrHospital of the University of Munich (LMU), Department of Anaesthesiology, Munich, Germany. Electronic address: alexander.chouker@med.uni-muenchen.de.
Institute of Biomedical Problems · RULMU Klinikum · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DE

Funding

Lymphatic Regulation of Skin Electrolyte Metabolism and Blood PressureR01HL118579 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI TITZE, JENS MARC · 2013 to 2017
$1.9M
NHLBI NIH HHS R01 HL118579
6 · The paper itself

Abstract

Increasing evidence indicated that excess salt consumption can impose risks on human health and a reduction in daily salt intake from the current average of approximately 12 g/d to 5-6 g/d was suggested by public health authorities. The studies on mice have revealed that sodium chloride plays a role in the modulation of the immune system and a high-salt diet can promote tissue inflammation and autoimmune disease. However, translational evidence of dietary salt on human immunity is scarce. We used an experimental approach of fixing salt intake of healthy human subjects at 12, 9, and 6 g/d for months and examined the relationship between salt-intake levels and changes in the immune system. Blood samples were taken from the end point of each salt intake period. Immune phenotype changes were monitored through peripheral leukocyte phenotype analysis. We assessed immune function changes through the characterization of cytokine profiles in response to mitogen stimulation. The results showed that subjects on the high-salt diet of 12 g/d displayed a significantly higher number of immune cell monocytes compared with the same subjects on a lower-salt diet, and correlation test revealed a strong positive association between salt-intake levels and monocyte numbers. The decrease in salt intake was accompanied by reduced production of proinflammatory cytokines interleukin (IL)-6 and IL-23, along with enhanced producing ability of anti-inflammatory cytokine IL-10. These results suggest that in healthy humans high-salt diet has a potential to bring about excessive immune response, which can be damaging to immune homeostasis, and a reduction in habitual dietary salt intake may induce potentially beneficial immune alterations.

Indexed as

AdultAnimalsAutoimmune DiseasesCytokinesHumansInflammationLeukocyte CountLongitudinal StudiesMaleMiceMonocytesRisk FactorsSodium Chloride, DietaryTranslational Research, BiomedicalVascular Endothelial Growth Factor CCytokinesSodium Chloride, DietaryVascular Endothelial Growth Factor C

Identifiers

PMID25497276
PMCPMC5538905
OpenAlexW2000613474

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.