Caffeine Inhibits NLRP3 Inflammasome Activation by Suppressing MAPK/NF-κB and A2aR Signaling in LPS-Induced THP-1 Macrophages
Zhao W, Ma L, Cai C, Gong X
International journal of biological sciences · 235 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- Science and Technology Commission of Shanghai Municipality
Based on 1 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2019-01-01 · Int J Biol Sci · vol. 15 · issue 8 · pp. 1571–1581
- Publisher
- Ivyspring International Publisher
- Cited
- 283 citations · more than 99% of similar papers · 11.2× the field average
- Impact
- Top 10% most cited in its field
- References
- 52 works
- Access
- Open access (journal) · CC-BY-NC
- Research areas
- Neonatal Respiratory Health Research · Inflammasome and immune disorders · Pediatric health and respiratory diseases
- Keywords
- Inflammasome, THP1 cell line, Caffeine, MAPK/ERK pathway, NF-κB, Chemistry, Signal transduction, Inflammation, Cell biology, AIM2, Pharmacology, Immunology, Medicine, Biology, Cell culture, Internal medicine
- MeSH
- humans, caffeine, mitogen-activated protein kinases, lipopolysaccharides, nf-kappa b, receptor, adenosine a2a, interleukin-18, interleukin-1beta, inflammasomes, nlr family, pyrin domain-containing 3 protein, thp-1 cells
4 authors
From CN
- Weiming ZhaoShanghai Jiao Tong University; Shanghai Children's Hospital
- Li MaShanghai Jiao Tong University; Shanghai Children's Hospital
- Cheng CaiShanghai Jiao Tong University; Shanghai Children's Hospital
- Xiaohui Gong · correspondingShanghai Jiao Tong University; Shanghai Children's Hospital
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY-NC).
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