Evidence map›Paper›PMID 30911044›Full record

ArticleScientific reports2019

Soy isoflavones and their metabolites modulate cytokine-induced natural killer cell function.

Thomas A Mace, Michael B Ware, Samantha A King, Shannon Loftus, Matthew R Farren, Elizabeth McMichael, Steven Scoville, Connor Geraghty, Gregory Young, William E Carson and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Thomas A MaceDivision of Gastroenterology Hepatology Nutrition, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Michael B WareDepartment of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, USA.
Samantha A KingDepartment of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Shannon LoftusDepartment of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Matthew R FarrenDepartment of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, USA.ORCID http://orcid.org/0000-0001-5510-8869
Elizabeth McMichaelDivision of Surgical Oncology, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Steven ScovilleBiomedical Sciences Graduate Program, Medical Scientist Training Program, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Connor GeraghtyDepartment of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Gregory YoungCenter for Biostatistics, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
William E CarsonDivision of Surgical Oncology, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Steven K ClintonDepartment of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA.
Gregory B LesinskiDepartment of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, USA. gregory.b.lesinski@emory.edu.
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USEmory University · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Jennifer A. Woyach · 1985 to 2026
$132.3M
Winship Cancer Institute Cancer Center Support GrantP30CA138292 · NCI · EMORY UNIVERSITY · PI Suresh S Ramalingam · 2009 to 2026
$47.5M
University of Iowa Clinical and Translational Science Program (TL1)UL1RR025755 · NCRR · OHIO STATE UNIVERSITY · PI JACKSON, REBECCA D · 2008 to 2011
$26.3M
ONOCOLOGY TRAINING GRANTT32CA009338 · NCI · OHIO STATE UNIVERSITY · PI BYRD, JOHN C., POLLOCK, RAPHAEL E. · 1985 to 2018
$8.3M
The Ohio State University Center for Clinical and Translational ScienceKL2TR001068 · NCATS · OHIO STATE UNIVERSITY · PI JACKSON, REBECCA D · 2013 to 2017
$2.7M
Modulation of antitumor immunity by dietary soy and its isoflavone constituentsR01CA169363 · NCI · OHIO STATE UNIVERSITY · PI CLINTON, STEVEN K, LESINSKI, GREGORY B. · 2013 to 2018
$1.6M
NCATS NIH HHS KL2 TR001068NCI NIH HHS P30 CA016058NCI NIH HHS P30 CA138292NCI NIH HHS R01 CA169363NCI NIH HHS T32 CA009338NCRR NIH HHS UL1 RR025755
6 · The paper itself

Abstract

Soybeans are a rich source of isoflavones that have been linked with anti-inflammatory processes and various health benefits. However, specific mechanisms whereby soy bioactives impact immune cell subsets are unclear. Isoflavones, such as genistein and daidzein, are metabolized by microbes to bioactive metabolites as O-desmethylangolensin (O-DMA) and equol, whose presence has been linked to health benefits. We examined how soy isoflavones and metabolites impact natural killer (NK) cell signaling and function. We observe no impact of isoflavones on viability of healthy donor peripheral blood mononuclear cells (PBMCs) or NK cells, even at high (25 µM) concentrations. However, pre-treatment of PBMCs with physiologically-relevant concentrations of genistein (p = 0.0023) and equol (p = 0.006) decreases interleukin (IL)-12/IL-18-induced interferon-gamma (IFN-γ) production versus controls. Detailed cellular analyses indicate genistein and equol decrease IL-12/IL-18-induced IFN-γ production by human NK cell subsets, but do not consistently alter cytotoxicity. At the level of signal transduction, genistein decreases IL-12/IL-18-induced total phosphorylated tyrosine, and phosphorylation MAPK pathway components. Further, genistein limits IL-12/IL-18-mediated upregulation of IL-18Rα expression on NK cells (p = 0.0109). Finally, in vivo studies revealed that C57BL/6 mice fed a soy-enriched diet produce less plasma IFN-γ following administration of IL-12/IL-18 versus control-fed animals (p < 0.0001). This study provides insight into how dietary soy modulates NK cell functions.

Indexed as

BiomarkersCell SurvivalCytokine-Induced Killer CellsCytokinesGene ExpressionGenisteinGlycine maxHumansImmunologic FactorsImmunomodulationImmunophenotypingIsoflavonesMolecular StructureSignal TransductionBiomarkersCytokinesGenisteinImmunologic FactorsIsoflavones

Identifiers

PMID30911044
PMCPMC6433892
OpenAlexW2923155507

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.