Evidence map›Paper›PMID 26384306›Full record

ArticleOncotarget2015

Caffeine affects the biological responses of human hematopoietic cells of myeloid lineage via downregulation of the mTOR pathway and xanthine oxidase activity.

Bernhard F Gibbs, Isabel Gonçalves Silva, Alexandr Prokhorov, Maryam Abooali, Inna M Yasinska, Maxwell A Casely-Hayford, Steffen M Berger, Elizaveta Fasler-Kan, Vadim V Sumbayev

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 21 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

9 authors at 4 institutions in 2 countries.

Bernhard F GibbsSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Isabel Gonçalves SilvaSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Alexandr ProkhorovSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Maryam AbooaliSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Inna M YasinskaSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Maxwell A Casely-HayfordSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Steffen M BergerDepartment of Pediatric Surgery and Department of Clinical Research, Inselspital, University Hospital, University of Bern, CH-3010 Bern, Switzerland.
Elizaveta Fasler-KanDepartment of Pediatric Surgery and Department of Clinical Research, Inselspital, University Hospital, University of Bern, CH-3010 Bern, Switzerland.
Vadim V SumbayevSchool of Pharmacy, University of Kent, Chatham Maritime, ME4 4TB Kent, United Kingdom.
Medway School of Pharmacy · GBUniversity of Kent · GBUniversity Hospital of Basel · CHUniversity Hospital of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Correction of human myeloid cell function is crucial for the prevention of inflammatory and allergic reactions as well as leukaemia progression. Caffeine, a naturally occurring food component, is known to display anti-inflammatory effects which have previously been ascribed largely to its inhibitory actions on phosphodiesterase. However, more recent studies suggest an additional role in affecting the activity of the mammalian target of rapamycin (mTOR), a master regulator of myeloid cell translational pathways, although detailed molecular events underlying its mode of action have not been elucidated. Here, we report the cellular uptake of caffeine, without metabolisation, by healthy and malignant hematopoietic myeloid cells including monocytes, basophils and primary acute myeloid leukaemia mononuclear blasts. Unmodified caffeine downregulated mTOR signalling, which affected glycolysis and the release of pro-inflammatory/pro-angiogenic cytokines as well as other inflammatory mediators. In monocytes, the effects of caffeine were potentiated by its ability to inhibit xanthine oxidase, an enzyme which plays a central role in human purine catabolism by generating uric acid. In basophils, caffeine also increased intracellular cyclic adenosine monophosphate (cAMP) levels which further enhanced its inhibitory action on mTOR. These results demonstrate an important mode of pharmacological action of caffeine with potentially wide-ranging therapeutic impact for treating non-infectious disorders of the human immune system, where it could be applied directly to inflammatory cells.

Indexed as

Cell LineageAngiogenic ProteinsBasophilsCaffeineCell Line, TumorCytokinesDose-Response Relationship, DrugDown-RegulationGlycolysisHumansInflammation MediatorsLeukemia, Myeloid, AcuteMonocytesMyeloid CellsSignal TransductionTOR Serine-Threonine KinasesAngiogenic ProteinsCaffeineCytokinesInflammation MediatorsMTOR protein, humanTOR Serine-Threonine KinasesXanthine OxidaseallergycaffeineImmune responseImmunityImmunology and Microbiology Sectioninflammationmyeloid cells

Identifiers

PMID26384306
PMCPMC4745685
OpenAlexW2187424361

What OpenQuestion holds

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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.