Evidence map›Paper›PMID 39840045›Full record

ArticleFrontiers in immunology2024

Apigenin inhibits NLRP3 inflammasome activation in monocytes and macrophages independently of CD38.

Knut Husø Lauritzen, Kuan Yang, Michael Frisk, Mieke C Louwe, Maria Belland Olsen, Mathias Ziegler, William E Louch, Bente Halvorsen, Pål Aukrust, Arne Yndestad and 1 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

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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

11 authors.

Knut Husø Lauritzen *Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Kuan Yang *Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Michael FriskInstitute for Experimental Medical Research, University of Oslo and Oslo University Hospital, Oslo, Norway.
Mieke C LouweResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Maria Belland OlsenResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Mathias ZieglerDepartment of Biomedicine, University of Bergen, Bergen, Norway.
William E LouchInstitute for Experimental Medical Research, University of Oslo and Oslo University Hospital, Oslo, Norway.
Bente HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Arne YndestadResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.
Øystein SandangerResearch Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet and University of Oslo, Oslo, Norway.

Funding

National Association for Public Health 1444Norwegian Research Council 240099/F20the South‐Eastern Norway Regional Health Authority 2018084the South‐Eastern Norway Regional Health Authority 2019067
6 · The paper itself

Abstract

Introduction: CD38, a regulator of intracellular calcium signalling, is highly expressed in immune cells. Mice lacking CD38 are very susceptible to acute bacterial infections, implicating CD38 in innate immune responses. The effects of CD38 inhibition on NLRP3 inflammasome activation in human primary monocytes and monocyte-derived macrophages have not been investigated. Apigenin is a naturally occurring flavonoid known to inhibit CD38. However, apigenin has also been proposed to inhibit the extracellular ATP receptor P2XR7, an upstream activator of NLRP3. In this study we aimed to investigate whether apigenin attenuates NLRP3 inflammasome activation in human monocytes and monocyte-derived macrophages through CD38 inhibition. Methods: LPS-primed human monocytes and monocyte-derived macrophages were treated with apigenin, the CD38 inhibitor 78c, antagonists of CD38 second messengers (8-br-ADPR and 8-br-cADPR) or the ATP hydrolase, apyrase, prior to NLRP3 activation with ATP, monosodium urate crystals (MSU) or nigericin. IL-1β and TNF secretion and mRNA expression, as well as N-terminal gasdermin-D formation were quantified. Ca Results: Apigenin significantly inhibited IL-1β release from LPS-primed monocytes and macrophages activated with ATP, MSU, or nigericin. CD38 inhibition with 78c also attenuated NLRP3-dependent IL-1β release. Apigenin was a potent inhibitor of Ca Discussion: Our data support that apigenin attenuates NLRP3 activation independently of CD38. Our results also suggest that MSU crystals activate NLRP3 through autocrine or paracrine ATP signalling.

Indexed as

ADP-ribosyl Cyclase 1ApigeninInflammasomesMacrophagesMembrane GlycoproteinsMonocytesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsCells, CulturedHumansLipopolysaccharidesMiceADP-ribosyl Cyclase 1ApigeninCD38 protein, humanInflammasomesLipopolysaccharidesMembrane GlycoproteinsNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanapigeninCD38inflammasomemacrophagemonocyteNLRP3

Identifiers

PMID39840045
PMCPMC11746122

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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.