Evidence map›Paper›PMID 12519385›Full record

ArticleClinical and experimental immunology2003

Nicotinamide is a potent inhibitor of proinflammatory cytokines.

J S Ungerstedt, M Blömback, T Söderström

2 registry-linked trialsOpen access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
2.4field-weighted citation impact, top 11% 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.

NCT06640309 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

The Effect of Nicotinamide on the Clinical Outcome of Rheumatoid Arthritis Patients

TypeinterventionalSponsorAin Shams UniversityRan2023 to 2025Enrolled70ConditionsRheumatoid ArthritisArmsNicotinamide Tablet, conventional synthetic antirheumatic drugs
NCT07655791 phase4not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Evaluation of the Efficacy and Safety of Oral Nicotinamide as an Adjunctive Therapy in Patients With Sepsis

TypeinterventionalSponsorAin Shams UniversityRan2026 to 2027Enrolled60ConditionsSepsis - to Reduce Mortality in the Intensive Care UnitArmsNicotinamide 1000 mg
3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 217 citations in OpenAlex.

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  4. Microvascular Dysfunction and Redox Imbalance in Long COVID.Microcirculation (New York, N.Y. : 1994) · 2026
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  6. Short-Term Alcohol Consumption Is Sufficient to Disrupt Microbial Communities and the Intestinal and Circulating Metabolites in a Non-Human Primate Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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30 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

3 authors at 1 institution in 1 country.

J S UngerstedtCoagulation Research, Department of Surgical Sciences, Karolinska Institutet, Stockholm, Sweden. johanna.ungerstedt@ks.se
M Blömback
T Söderström
Karolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study investigates the modulating effects of nicotinamide on the cytokine response to endotoxin. In an in vitro model of endotoxaemia, human whole blood was stimulated for two hours with endotoxin at 1 ng/ml, achieving high levels of the proinflammatory cytokines IL-1 beta, IL-6, IL-8 and TNF alpha. When coincubating whole blood, endotoxin and the vitamin B3 derivative nicotinamide, all four cytokines measured were inhibited in a dose dependent manner. Inhibition was observed already at a nicotinamide concentration of 2 mmol/l. At a concentration of 40 mmol/l, the IL-1 beta, IL-6 and TNF alpha responses were reduced by more than 95% and the IL-8 levels reduced by 85%. Endotoxin stimulation activates poly(ADP-ribose)polymerase (PARP), a nuclear DNA repair enzyme. It has been hypothesized that the anti-inflammatory properties of nicotinamide are due to PARP inhibition. In the present study, the endotoxin induced PARP activation was dose dependently decreased with 4-40 mmol/l nicotinamide or 4-100 micro mol/l 6(5H) phenanthridinone, a specific PARP inhibitor. 6(5H)phenanthridinone however, failed to inhibit the proinflammatory cytokines. Thus, the mechanism behind the cytokine inhibition in our model seems not to be due to PARP inhibition. In conclusion, the present study could not only confirm previous reports of a down-regulatory effect on TNFalpha, but demonstrates that nicotinamide is a potent modulator of several proinflammatory cytokines. These findings demonstrate that nicotinamide has a potent immunomodulatory effect in vitro, and may have great potential for treatment of human inflammatory disease.

Indexed as

Adjuvants, ImmunologicCells, CulturedCytokinesDepression, ChemicalDose-Response Relationship, DrugEndotoxemiaEnzyme InhibitorsHumansInterleukin-1Interleukin-6Interleukin-8NiacinamidePhenanthrenesPoly Adenosine Diphosphate RiboseTumor Necrosis Factor-alphaAdjuvants, ImmunologicCytokinesEnzyme InhibitorsInterleukin-1Interleukin-6Interleukin-8NiacinamidePhenanthrenesphenanthridonePoly Adenosine Diphosphate RiboseTumor Necrosis Factor-alpha

Identifiers

PMID12519385
PMCPMC1808598
OpenAlexW2163059346

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.