Evidence map›Paper›PMID 28377398›Full record

ArticleJournal of leukocyte biology2017

IL-27 enhances LPS-induced IL-1β in human monocytes and murine macrophages.

Carlene Petes, Christopher Wynick, Christina Guzzo, Divya Mehta, Sarah Logan, Bruce W Banfield, Sameh Basta, Andrea Cooper, Katrina Gee

Open access · bronzeAbstract read
In one paragraph

Article in Journal of leukocyte biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

  1. Immunomodulatory Effects ofInternational journal of molecular sciences · 2026
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  11. Contribution of Invariant Natural Killer T Cells to the Clearance ofInternational journal of molecular sciences · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. IL-27: An endogenous constitutive repressor of human monocytes.Clinical immunology (Orlando, Fla.) · 2020
    Article
  18. Interleukin-27 Functional Duality BalancesFrontiers in immunology · 2020
    Review
  19. Review
  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

9 authors at 3 institutions in 3 countries.

Carlene PetesDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Christopher WynickDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Christina GuzzoDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Divya MehtaDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Sarah LoganDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Bruce W BanfieldDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Sameh BastaDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada.
Andrea CooperDepartment of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom.
Katrina GeeDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada; kgee@queensu.ca.
Queen's University · CANational Institute of Allergy and Infectious Diseases · USUniversity of Leicester · GB

Funding

Medical Research Council MR/P011136/1
6 · The paper itself

Abstract

IL-27 bridges innate and adaptive immunity by modulating cytokine production from myeloid cells and regulating Th cell differentiation. During bacterial infection, TLR4 triggering by LPS induces IL-27 production by monocytes and macrophages. We have previously shown that IL-27 can prime monocytes for LPS responsiveness by enhancing TLR4 expression and intracellular signaling. If unregulated, this could result in damaging inflammation, whereas on the other hand, this may also provide greater responses by inflammatory processes induced in response to bacterial pathogens. A key process in fine-tuning inflammatory responses is activation of the inflammasome, which ultimately results in IL-1β production. Herein, we investigated the molecular mechanisms by which IL-27 modulates LPS-induced IL-1β secretion in monocytes and macrophages. We found that when delivered simultaneously with LPS, IL-27 augments activation of caspase-1 and subsequent release of IL-1β. Furthermore, we determined that IL-27 primes cells for enhanced IL-1β production by up-regulating surface expression of TLR4 and P2X purinoceptor 7 (P2X7) for enhanced LPS and ATP signaling, respectively. These findings provide new evidence that IL-27 plays an important role in the proinflammatory capacity of monocytes and macrophages via enhancing IL-1β secretion levels triggered by dual LPS-ATP stimulation.

Indexed as

Adenosine TriphosphateAnimalsCaspase 1Cell Line, TumorHumansInterleukin-1betaInterleukinsLipopolysaccharidesMacrophagesMiceMice, KnockoutMonocytesReceptors, Purinergic P2X7Signal TransductionToll-Like Receptor 4Adenosine TriphosphateCaspase 1IL1B protein, humanIL1B protein, mouseIl27 protein, mouseInterleukin-1betaInterleukinsLipopolysaccharidesMYDGF protein, humanP2RX7 protein, humanReceptors, Purinergic P2X7TLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4inflammasomeinflammationinnate immunitylipopolysaccharideToll-like receptor

Identifiers

PMID28377398
PMCPMC6608054
OpenAlexW2604952534

What OpenQuestion holds

Textmetadata
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.