Evidence map›Paper›PMID 18779392›Full record

ArticleBlood2008

Resolution-phase macrophages possess a unique inflammatory phenotype that is controlled by cAMP.

Jonas Bystrom, Ian Evans, Justine Newson, Melanie Stables, Iqbal Toor, Nico van Rooijen, Mark Crawford, Paul Colville-Nash, Stuart Farrow, Derek W Gilroy

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01379950 (The Role of Macrophages in the Inflammatory Resolution Phase in Periodontal Patients), which is not on this map. Cited by 166 papers.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed
4.5field-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.

NCT01379950 unknown statusnot on this mapstarted 2011, after this paper: background citation

The Role of Macrophages in the Inflammatory Resolution Phase in Periodontal Patients

TypeobservationalSponsorHadassah Medical OrganizationRan2011 to 2012Enrolled30ConditionsPeriodontitis
3 · Its place in the literature

Who cites it

166 citing papers in PubMed, 331 citations in OpenAlex.

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  18. Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025
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106 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

10 authors at 5 institutions in 3 countries.

Jonas BystromCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom.
Ian Evans
Justine Newson
Melanie Stables
Iqbal Toor
Nico van Rooijen
Mark Crawford
Paul Colville-Nash
Stuart Farrow
Derek W Gilroy
Therapeutics Clinical Research · USUniversity College London · GBGlaxoSmithKline (United Kingdom) · GBSt Helier Hospital · GBVrije Universiteit Amsterdam · NL

Funding

Medical Research Council G0800758Wellcome Trust
6 · The paper itself

Abstract

Neutralizing injurious stimuli, proinflammatory mediator catabolism, and polymorphonuclear leukocyte (PMN) clearance are determinants of inflammatory resolution. To this, we recently added innate-type lymphocyte repopulation as being central for restoring postinflammation tissue homeostasis with a role in controlling innate immune-mediated responses to secondary infection. However, although macrophages dominate resolution, their phenotype and role in restoring tissue physiology once inflammation abates are unknown. Therefore, we isolated macrophages from the resolving phase of acute inflammation and found that compared with classically activated proinflammatory M1 cells, resolution-phase macrophages (rMs) possess weaker bactericidal properties and express an alternatively activated phenotype but with elevated markers of M1 cells including inducible cyclooxygenase (COX 2) and nitric oxide synthase (iNOS). This phenotype is controlled by cAMP, which, when inhibited, transforms rM to M1 cells. Conversely, elevating cAMP in M1 cells transforms them to rMs, with implications for cAMP in the resolution of systemic inflammation. It transpires that although rMs are dispensable for clearing PMNs during self-limiting inflammation, they are essential for signaling postresolution lymphocyte repopulation via COX 2 lipids. Thus, rM macrophages are neither classically nor alternatively activated but a hybrid of both, with a role in mediating postresolution innate-lymphocyte repopulation and restoring tissue homeostasis.

Indexed as

Immunity, InnateMacrophage ActivationAnimalsCyclic AMPCyclooxygenase 2HomeostasisInflammationLymphocytesMacrophages, PeritonealMiceNitric Oxide Synthase Type IIRecovery of FunctionCyclic AMPCyclooxygenase 2Nitric Oxide Synthase Type IINos2 protein, mousePtgs2 protein, mouse

Identifiers

PMID18779392
PMCPMC2581990
OpenAlexW2065769697

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

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.