Evidence map›Paper›PMID 12368905›Full record

ArticleNature medicine2002

Endogenous lipid- and peptide-derived anti-inflammatory pathways generated with glucocorticoid and aspirin treatment activate the lipoxin A4 receptor.

Mauro Perretti, Nan Chiang, Mylinh La, Iolanda M Fierro, Stefano Marullo, Stephen J Getting, Egle Solito, Charles N Serhan

Open access · greenAbstract read
In one paragraph

Article in Nature medicine, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 201 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
201citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

201 citing papers in PubMed, 1 synthesis or guideline pooled it, 445 citations in OpenAlex.

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141 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

8 authors at 4 institutions in 3 countries.

Mauro Perretti[1] Department of Biochemical Pharmacology, William Harvey Research Institute, Bart's and The London School of Medicine, Queen Mary University of London, Charterhouse Square, London, UK [2] M.P. and N.C. contributed equally to this paper.
Nan Chiang
Mylinh La
Iolanda M Fierro
Stefano Marullo
Stephen J Getting
Egle Solito
Charles N Serhan
Brigham and Women's Hospital · USQueen Mary University of London · GBImperial College London · GBInstitut Gustave Roussy · FR

Funding

Novel anti-inflamatory lipid mediatorsP01DE013499 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SERHAN, CHARLES NICHOLAS · 2000 to 2004
$5.3M
BLOOD CELL LIPOXYGENASE PRODUCTS: FORMATION AND ACTIONR01GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1992 to 2020
$4.9M
BLOOD CELL LIPOXYGENASE PRODUCTS--FORMATION AND ACTIONR37GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 2000 to 2009
$4.0M
BLOOD CELL LIPOXYGENASE PRODUCTS--FORMATION &ACTIONR29GM038765 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI SERHAN, CHARLES NICHOLAS · 1987 to 1991
–
Arthritis Research UK 15755NIDCR NIH HHS P01 DE013499NIDCR NIH HHS P01-DE13499NIGMS NIH HHS GM38765NIGMS NIH HHS R01 GM038765NIGMS NIH HHS R37 GM038765
6 · The paper itself

Abstract

Aspirin (ASA) and dexamethasone (DEX) are widely used anti-inflammatory agents yet their mechanism(s) for blocking polymorphonuclear neutrophil (PMN) accumulation at sites of inflammation remains unclear. Here, we report that inhibition of PMN infiltration by ASA and DEX is a property shared by aspirin-triggered lipoxins (ATL) and the glucocorticoid-induced annexin 1 (ANXA1)-derived peptides that are both generated in vivo and act at the lipoxin A(4) receptor (ALXR/FPRL1) to halt PMN diapedesis. These structurally diverse ligands specifically interact directly with recombinant human ALXR demonstrated by specific radioligand binding and function as well as immunoprecipitation of PMN receptors. In addition, the combination of both ATL and ANXA1-derived peptides limited PMN infiltration and reduced production of inflammatory mediators (that is, prostaglandins and chemokines) in vivo. Together, these results indicate functional redundancies in endogenous lipid and peptide anti-inflammatory circuits that are spatially and temporally separate, where both ATL and specific ANXA1-derived peptides act in concert at ALXR to downregulate PMN recruitment to inflammatory loci.

Indexed as

Lipid MetabolismReceptors, Formyl PeptideReceptors, LipoxinAnimalsAnti-Inflammatory AgentsAspirinCell LineCells, CulturedDexamethasoneHumansIn Vitro TechniquesMiceMolecular Sequence DataNeutrophil ActivationPeptidesReceptors, Cell SurfaceAnti-Inflammatory AgentsAspirinDexamethasoneFPR2 protein, humanPeptidesReceptors, Cell SurfaceReceptors, Formyl PeptideReceptors, Lipoxin

Identifiers

PMID12368905
PMCPMC2777269
OpenAlexW1982283061

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.