Evidence map›Paper›PMID 27499924›Full record

ArticleThe journal of pathology. Clinical research2016

Novel translational model of resolving inflammation triggered by UV-killed E. coli.

Madhur P Motwani, Julia D Flint, Roel Ph De Maeyer, James N Fullerton, Andrew M Smith, Daniel Jb Marks, Derek W Gilroy

Open access · goldAbstract read
In one paragraph

Article in The journal of pathology. Clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.9field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  18. UV radiation recruits CD4Clinical & translational immunology · 2020
    Article
  19. Ajulemic acid: potential treatment for chronic inflammation.Pharmacology research & perspectives · 2018
    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

7 authors at 2 institutions in 1 country.

Madhur P MotwaniCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street University College London London WC1E 6JF UK.
Julia D FlintCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street University College London London WC1E 6JF UK.
Roel Ph De MaeyerCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street University College London London WC1E 6JF UK.
James N FullertonCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street University College London London WC1E 6JF UK.
Andrew M SmithMicrobial Diseases, Eastman Dental Institute, University College London London WC1X 8LD UK.
Daniel Jb MarksCentre for Molecular Medicine, Division of Medicine, 5 University Street University College London London WC1E 6JF UK.
Derek W GilroyCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, 5 University Street University College London London WC1E 6JF UK.
University College London · GBEastman Dental Hospital · GB

Funding

Medical Research Council MR/L000261/1Wellcome Trust
6 · The paper itself

Abstract

Whilst numerous studies investigating the aetiology of inflammatory diseases have been performed in rodents, the applicability of these data to human pathophysiology is frequently debated. Regardless of the strengths and weaknesses of rodent models in biomedical research, there is a need to develop models of experimental inflammation in humans. Here, we describe a self-resolving acute inflammatory response triggered by the intradermal injection of UV-killed Escherichia coli into the forearm of healthy volunteers. Cells and exudates were harvested from onset to resolution by applying negative pressure over the inflamed site. Onset was characterized by high blood flow, neutrophilia and peak levels of pro-inflammatory cytokines, whilst resolution showed a decline in blood blow, reduction in neutrophils, increase in monocytes/macrophages and waning of classic pro-inflammatory cytokine levels. An anti-inflammatory effect, defined as suppression of onset phase events, was demonstrated by administering naproxen, a conventional non-steroidal anti-inflammatory drug. In summary, this model of resolving acute inflammation is minimally invasive, highly tractable and allows simultaneous investigation of the vascular response, cellular trafficking and chemical mediator profile of onset and resolution phases of acute inflammation in humans. It can serve as a translational platform to provide mechanistic insights and to test the clinical efficacy of novel anti-inflammatory and pro-resolving drugs, and also as a tool in patients to explore inherent defects in resolution pathways.

Indexed as

human in vivo modelmacrophageneutrophilresolution of inflammationtranslational research

Identifiers

PMID27499924
PMCPMC4958736
OpenAlexW2337809778

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.