Evidence map›Paper›PMID 24846290›Full record

Trial reportPloS one2014

Serum amyloid A induces NLRP-3-mediated IL-1β secretion in neutrophils.

Kiyoshi Migita, Yasumori Izumi, Yuka Jiuchi, Hideko Kozuru, Chieko Kawahara, Minoru Nakamura, Tadashi Nakamura, Kazunaga Agematsu, Junya Masumoto, Michio Yasunami and 2 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Evaluating theFrontiers in immunology · 2026
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  6. The Role ofBiomolecules · 2025
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  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Role of the renin-angiotensin system in NETosis in the coronavirus disease 2019 (COVID-19).Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022
    Review
  17. Review
  18. Review
  19. Article
  20. Article
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

12 authors at 6 institutions in 1 country.

Kiyoshi MigitaDepartment of Rheumatology and Clinical Research Center, Nagasaki Medical Center, Omura, Nagasaki, Japan.
Yasumori IzumiDepartment of Rheumatology and Clinical Research Center, Nagasaki Medical Center, Omura, Nagasaki, Japan.
Yuka JiuchiDepartment of Rheumatology and Clinical Research Center, Nagasaki Medical Center, Omura, Nagasaki, Japan.
Hideko KozuruDepartment of Rheumatology and Clinical Research Center, Nagasaki Medical Center, Omura, Nagasaki, Japan.
Chieko KawaharaDepartment of Rheumatology and Clinical Research Center, Nagasaki Medical Center, Omura, Nagasaki, Japan.
Minoru NakamuraDepartment of Rheumatology and Clinical Research Center, Nagasaki Medical Center, Omura, Nagasaki, Japan.
Tadashi NakamuraDepartment of Rheumatology, Shinto Kumamoto Hospital, Kumamoto, Japan.
Kazunaga AgematsuDepartment of Infection and Host Defense, Graduate School of Medicine, Shinshu University, Matsumoto, Nagano, Japan.
Junya MasumotoDepartment of Pathology, Ehime University Graduate School of Medicine and Proteo-Science Center, Toon, Ehime, Japan.
Michio YasunamiInstitute of Tropical Medicine (NEKKEN), Nagasaki University, Nagasaki University, Nagasaki, Japan.
Atsushi KawakamiDepartment of Rheumatology, Nagasaki University Hospital, Nagasaki, Japan.
Katsumi EguchiDepartment of Rheumatology, Sasebo City General Hospital, Sasebo, Nagasaki, Japan.
Nagasaki Medical Center · JPEhime University · JPNagasaki University · JPNagasaki University Hospital · JPSasebo City General Hospital · JPShinshu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimsSerum amyloid A (SAA) is an acute phase reactant with significant immunological activities, including effects on cytokine synthesis and neutrophil chemotaxis. Neutrophils can also release cytokines with proinflammatory properties. IL-1β is a key proinflammatory cytokine, the secretion of which is controlled by inflammasome. We investigated the proinflammatory effects of SAA in vitro in relation to the NLRP3 inflammasome in neutrophils. METHODOLOGY/PRINCIPAL

findingsHuman neutrophils isolated form healthy subjects were stimulated with serum amyloid A (SAA). The cellular supernatants were analyzed by western blot using anti-IL-1β or anti-caspase-1 antibodies. IL-1β or Nod-like receptor family, pyrin domain containing 3 (NLRP3) mRNA expressions were analyzed by real-time PCR or reverse transcription-PCR (RT-PCR) method. SAA stimulation induced pro-IL-1β mRNA expression in neutrophils. Furthermore, SAA engaged the caspase-1-activating inflammasome, resulting in the production of active IL-1β. SAA-induced pro-IL-1β expression was marginally suppressed by the Syk specific inhibitor, R406, and SAA-induced pro-IL-1β processing in neutrophils was prevented by R406. Furthermore, SAA-induced NLRP3 mRNA expression was completely blocked by R406. Analysis of intracellular signaling revealed that SAA stimulation activated the tyrosine kinase Syk and mitogen-activated protein kinase (MAPK). CONCLUSIONS/SIGNIFICANCE: These results demonstrate that the innate neutrophil immune response against SAA involves a two-step activation process: an initial signal promoting expression of pro-IL-1β and a second signal involving Syk-dependent activation of the NLRP3 inflammasome and caspase-1, allowing processing of pro-IL-1β and secretion of mature IL-1β.

Indexed as

Carrier ProteinsCaspase 1Extracellular Signal-Regulated MAP KinasesFemaleHumansInflammasomesInterleukin-1betaIntracellular Signaling Peptides and ProteinsMaleNeutrophil ActivationNeutrophilsNLR Family, Pyrin Domain-Containing 3 ProteinOxazinesProtein-Tyrosine KinasesPyridinesSerum Amyloid A ProteinCarrier ProteinsCaspase 1Extracellular Signal-Regulated MAP KinasesIL1B protein, humanInflammasomesInterleukin-1betaIntracellular Signaling Peptides and ProteinsN4-(2,2-dimethyl-3-oxo-4H-pyrid(1,4)oxazin-6-yl)-5-fluoro-N2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamineNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanOxazinesProtein-Tyrosine KinasesPyridinesSerum Amyloid A ProteinSyk KinaseSYK protein, human

Identifiers

PMID24846290
PMCPMC4028190
OpenAlexW2031521774

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.