Evidence map›Paper›PMID 20421472›Full record

Trial reportProceedings of the National Academy of Sciences of the United States of America2010

Dichotomy in duration and severity of acute inflammatory responses in humans arising from differentially expressed proresolution pathways.

Thea Morris, Melanie Stables, Paul Colville-Nash, Justine Newson, Geoffrey Bellingan, Patricia M de Souza, Derek W Gilroy

Abstract readClinical Trial
In one paragraph

Trial report in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023
    Review
  5. Article
  6. Review
  7. Changes of lipoxin levels during pregnancy and the monthly-cycle, condition the normal course of pregnancy or pathology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Review
  8. Article
  9. Review
  10. Lipid mediators in immune regulation and resolution.British journal of pharmacology · 2019
    Review
  11. Aspirin-triggered proresolving mediators stimulate resolution in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. PDCell chemical biology · 2018
    Article
  17. Review
  18. Review
  19. Article
  20. Article

9 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

7 authors at 3 institutions in 2 countries.

Thea MorrisCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London WC1E 6JJ, UK.
Melanie Stables
Paul Colville-Nash
Justine Newson
Geoffrey Bellingan
Patricia M de Souza
Derek W Gilroy
University College London · GBImperial College London · GBSt Helier Hospital · GB

Funding

Medical Research Council G0500017Wellcome Trust 087520
6 · The paper itself

Abstract

Lipoxins (Lxs) and aspirin-triggered epi-Lxs (15-epi-LxA(4)) act through the ALX/FPRL1 receptor to block leukocyte trafficking, dampen cytokine/chemokine synthesis, and enhance phagocytic clearance of apoptotic leukocytes-key requisites for inflammatory resolution. Although studies using primarily inbred rodents have highlighted resolution as an active event, little is known about the role resolution pathways play in controlling the duration/profile of inflammatory responses in humans. To examine this, we found two types of responders to cantharidin-induced skin blisters in male healthy volunteers: those with immediate leukocyte accumulation and cytokine/chemokine synthesis followed by early resolution and a second group whose inflammation increased gradually over time followed by delayed resolution. In early resolvers, blister 15-epi-LxA(4) and leukocyte ALX were low, but increased as inflammation abated. In contrast, in delayed resolvers, 15-epi-LxA(4) and ALX were high early in the response but waned as inflammation progressed. Elevating 15-epi-LxA(4) in early resolvers using aspirin increased blister leukocyte ALX but reduced cytokines/chemokines as well as polymorphonuclear leukocyte and macrophage numbers. These findings show that two phenotypes exist in humans with respect to inflammation severity/longevity controlled by proresolution mediators, namely 15-epi-LxA(4). These data have implications for understanding the etiology of chronic inflammation and future directions in antiinflammatory therapy.

Indexed as

AdultAspirinHumansInflammationLipoxinsMaleMiddle AgedReceptors, Formyl PeptideReceptors, LipoxinTime FactorsAspirinFPR2 protein, humanlipoxin A4LipoxinsReceptors, Formyl PeptideReceptors, Lipoxin

Identifiers

PMID20421472
PMCPMC2889345
OpenAlexW2075780068

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.