Evidence map›Paper›PMID 31360100›Full record

ArticleInternational journal of biological sciences2019

Caffeine Inhibits NLRP3 Inflammasome Activation by Suppressing MAPK/NF-κB and A2aR Signaling in LPS-Induced THP-1 Macrophages.

Weiming Zhao, Li Ma, Cheng Cai, Xiaohui Gong

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 1 pooled it
12.7field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 1 synthesis or guideline pooled it, 264 citations in OpenAlex.

  1. Pooled it
  2. From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
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  18. IL-18-Mediated Tumor Immune Evasion.Current issues in molecular biology · 2026
    Review
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  20. Article

87 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

4 authors at 2 institutions in 1 country.

Weiming ZhaoDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Li MaDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Cheng CaiDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Xiaohui GongDepartment of Neonatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, China.
Shanghai Children's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive inflammation induced by various risk factors is associated with the development of bronchopulmonary dysplasia (BPD). Caffeine exerts potent anti-inflammatory effects as a clinical preventive medicine for BPD. Recently, NLRP3 inflammasome activation has been demonstrated to be essential for the pathogenesis of BPD. In the present study, we aimed to investigate the effects of caffeine on NLRP3 inflammasome activation in LPS-induced THP-1 macrophages and to explore the underlying the detailed mechanism. We found that caffeine significantly reduced NLRP3 expression, ASC speck formation, and caspase 1 cleavage and therefore decreased IL-1β and IL-18 secretion in THP-1 macrophages. Caffeine also markedly decreased the phosphorylation levels of MAPK and NF-κB pathway members, further suppressing the translocation of NF-κB in THP-1 macrophages. Moreover, silencing of the caffeine-antagonized adenosine A2a receptor (A2aR) significantly decreased cleaved caspase 1 expression in THP-1 macrophages by reducing ROS production. Given these findings, we conclude that caffeine inhibits NLRP3 inflammasome activation by suppressing MAPK/NF-κB signaling and A2aR-associated ROS production in LPS-induced THP-1 macrophages.

Indexed as

CaffeineHumansInflammasomesInterleukin-18Interleukin-1betaLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReceptor, Adenosine A2ATHP-1 CellsCaffeineInflammasomesInterleukin-18Interleukin-1betaLipopolysaccharidesMitogen-Activated Protein KinasesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReceptor, Adenosine A2AA2aRCaffeineMAPKNF-κBNLRP3 inflammasomeTHP-1 macrophages

Identifiers

PMID31360100
PMCPMC6643212
OpenAlexW2950111581

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.