Evidence map›Paper›PMID 26764408›Full record

ArticleBioscience reports2016

Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages.

Abbas Jawad Al-Shabany, Alan John Moody, Andrew David Foey, Richard Andrew Billington

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Nicotinamide Mononucleotide Restores NADAntioxidants (Basel, Switzerland) · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Inflammatory Mechanism ofInternational journal of molecular sciences · 2022
    Review
  15. Article
  16. Heme oxygenase-1 protects against endotoxin-induced acute lung injury depends on NADInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  17. Article
  18. Local Targeting of NADCancer research · 2020
    Article
  19. Article
  20. Review
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

4 authors at 1 institution in 1 country.

Abbas Jawad Al-ShabanySchool of Biological Sciences, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, U.K.
Alan John MoodySchool of Biological Sciences, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, U.K.
Andrew David FoeySchool of Biomedical and Healthcare Sciences, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, U.K.
Richard Andrew BillingtonSchool of Biological Sciences, University of Plymouth, Drake Circus, Plymouth, PL4 8AA, U.K. richard.billington@plymouth.ac.uk.
University of Plymouth · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolism and immune responses have been shown to be closely linked and as our understanding increases, so do the intricacies of the level of linkage. NAD(+) has previously been shown to regulate tumour necrosis factor-α (TNF-α) synthesis and TNF-α has been shown to regulate NAD(+) homoeostasis providing a link between a pro-inflammatory response and redox status. In the present study, we have used THP-1 differentiation into pro- (M1-like) and anti- (M2-like) inflammatory macrophage subset models to investigate this link further. Pro- and anti-inflammatory macrophages showed different resting NAD(+) levels and expression levels of NAD(+) homoeostasis enzymes. Challenge with bacterial lipopolysaccharide, a pro-inflammatory stimulus for macrophages, caused a large, biphasic and transient increase in NAD(+) levels in pro- but not anti-inflammatory macrophages that were correlated with TNF-α release and inhibition of certain NAD(+) synthesis pathways blocked TNF-α release. Lipopolysaccharide stimulation also caused changes in mRNA levels of some NAD(+) homoeostasis enzymes in M1-like cells. Surprisingly, despite M2-like cells not releasing TNF-α or changing NAD(+) levels in response to lipopolysaccharide, they showed similar mRNA changes compared with M1-like cells. These data further strengthen the link between pro-inflammatory responses in macrophages and NAD(+). The agonist-induced rise in NAD(+) shows striking parallels to well-known second messengers and raises the possibility that NAD(+) is acting in a similar manner in this model.

Indexed as

Cell Line, TumorHumansInflammationLipopolysaccharidesMacrophagesNADTumor Necrosis Factor-alphaLipopolysaccharidesNADTumor Necrosis Factor-alphaimmune responseslipopolysaccharide (LPS)macrophagespyridine nucleotidessecond messengerTNF-α

Identifiers

PMID26764408
PMCPMC4770305
OpenAlexW2249724383

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.