Evidence map›Paper›PMID 26878867›Full record

ArticleInnate immunity2016

Resolvin D1, resolvin D2 and maresin 1 activate the GSK3β anti-inflammatory axis in TLR4-engaged human monocytes.

Zhen Gu, Gwyneth J Lamont, Richard J Lamont, Silvia M Uriarte, Huizhi Wang, David A Scott

Open access · bronzeAbstract read
In one paragraph

Article in Innate immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Transcriptional regulation and function of GPR18 in macrophage subtype specification.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Docosahexaenoic acid supplementation inhibits monocyte exhaustion memory formation during sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Resolvin D2 restores monocyte anisocytosis and mediates a shift toward classical monocytes ex vivo in blood samples from patients after major burns.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
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  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

6 authors at 1 institution in 1 country.

Zhen GuDepartment of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY, USA.
Gwyneth J LamontDepartment of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY, USA.
Richard J LamontDepartment of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY, USA.
Silvia M UriarteDepartment of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY, USA Department of Medicine, University of Louisville, KY, USA.
Huizhi WangDepartment of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY, USA.
David A ScottDepartment of Oral Immunology and Infectious Diseases, University of Louisville, Louisville, KY, USA david.scott@louisville.edu.
University of Louisville · US

Funding

P GINGIVALIS INTERACTIONS WITH GINGIVAL EPITHELIAL CELLSR01DE011111 · NIDCR · UNIVERSITY OF WASHINGTON · PI HARIBABU BODDULURI, Richard J Lamont · 1995 to 2026
$5.4M
Filifactor alocis interactions with neutrophilsR01DE024509 · NIDCR · UNIVERSITY OF LOUISVILLE · PI URIARTE, SILVIA M · 2014 to 2023
$4.2M
P.gingivalis Interactions with Gingival Epithelial CellsR37DE011111 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2009 to 2018
$3.6M
Role of GSK3 in host inflammationR01DE017680 · NIDCR · UNIVERSITY OF LOUISVILLE · PI SCOTT, DAVID A · 2007 to 2017
$3.3M
Role of JAKs in innate responses to P. gingivalisR01DE017921 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2010 to 2019
$3.3M
Tobacco-induced alterations to P. gingivalis-host interactionsR01DE019826 · NIDCR · UNIVERSITY OF LOUISVILLE · PI SCOTT, DAVID A · 2010 to 2014
$1.8M
SGK1 is a Central Regulator of P. gingivalis-Induced InflammationR21DE023633 · NIDCR · UNIVERSITY OF LOUISVILLE · PI WANG, HUIZHI · 2013 to 2014
$413k
NIDCR NIH HHS DE011111NIDCR NIH HHS DE017680NIDCR NIH HHS DE017921NIDCR NIH HHS DE023633NIDCR NIH HHS DE025409NIDCR NIH HHS R01 DE011111NIDCR NIH HHS R01 DE017680NIDCR NIH HHS R01 DE017921NIDCR NIH HHS R01 DE019826NIDCR NIH HHS R01 DE024509NIDCR NIH HHS R21 DE023633NIDCR NIH HHS R37 DE011111
6 · The paper itself

Abstract

Pro-resolving, docosahexaenoic acid-derived mediators have recently emerged as important potential therapeutic agents for the amelioration of complications arising from inflammation, such as vascular disease, asthma, acute lung injury and colitis. While resolvin D1 (RVD1), resolvin D2 (RVD2) and maresin 1 (MaR1) are established pro-resolvins, their mechanisms of action remain unclear. Here we show that, in LPS-stimulated primary human monocytes, RVD1, RVD2 and MaR1 each suppress the release of pro-inflammatory cytokines (TNF, IL-1β, IL-8) and the innate/adaptive bridging cytokine, IL-12 p40, while simultaneously augmenting the production of the anti-inflammatory cytokine, IL-10. Such resolving activity is accompanied by the increased phosphorylation (enhanced anti-inflammatory state) of glycogen synthase kinase 3β (GSK3β) along with increased phosphorylation (activation) of Akt, SGK1 and CREB but not MAPK-related molecules. Gain and loss of function experiments confirm a key role for GSK3β and CREB in the anti-inflammatory actions of resolvins. These results suggest that induction of the GSK3β anti-inflammatory axis is a common mechanism of action for RVD1, RVD2 and MaR1.

Indexed as

Anti-Inflammatory AgentsCells, CulturedCyclic AMP Response Element-Binding ProteinCytokinesDocosahexaenoic AcidsGlycogen Synthase Kinase 3 betaHumansImmediate-Early ProteinsIndolesInflammationLipopolysaccharidesMaleimidesMonocytesPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-akt7,14-dihydroxydocosa-4,8,10,12,16,19-hexaenoic acidAnti-Inflammatory AgentsCREB1 protein, humanCyclic AMP Response Element-Binding ProteinCytokinesDocosahexaenoic AcidsGlycogen Synthase Kinase 3 betaImmediate-Early ProteinsIndolesLipopolysaccharidesMaleimidesProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktresolvin D1resolvin D2RNA, Small InterferingSB 216763Serum-Glucocorticoid Regulated KinasesTLR4 protein, humanToll-Like Receptor 4CREBGSK3βinflammationLPSmaresinresolvin

Identifiers

PMID26878867
PMCPMC5257244
OpenAlexW2287654917

What OpenQuestion holds

Textmetadata
LicenceTDM
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.