Evidence map›Paper›PMID 29073216›Full record

ArticlePloS one2017

Prolonged immune alteration following resolution of acute inflammation in humans.

Madhur P Motwani, Justine Newson, Simon Kwong, Angela Richard-Loendt, Romain Colas, Jesmond Dalli, Derek W Gilroy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

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  14. Skin Cancer Microenvironment: What We Can Learn from Skin Aging?International journal of molecular sciences · 2023
    Review
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  16. Article
  17. Photoaging: UV radiation-induced inflammation and immunosuppression accelerate the aging process in the skin.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  18. Clinical perspectives on the age-related increase of immunosuppressive activity.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Madhur P MotwaniCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom.ORCID http://orcid.org/0000-0001-6970-897X
Justine NewsonCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom.
Simon KwongCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom.
Angela Richard-LoendtDivision of Neuropathology and, Dept. of Neurodegenerative Disease, University College London Institute of Neurology, Queen Square, London, United Kingdom.
Romain ColasLipid Mediator Unit, William Harvey Research Institute, Bart's and the London School of Medicine, Queen Mary University of London, London, United Kingdom.
Jesmond DalliLipid Mediator Unit, William Harvey Research Institute, Bart's and the London School of Medicine, Queen Mary University of London, London, United Kingdom.
Derek W GilroyCentre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, London, United Kingdom.
University College London · GBQueen Mary University of London · GBNational Hospital for Neurology and Neurosurgery · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Acute inflammation is an immediate response to infection and injury characterised by the influx of granulocytes followed by phagocytosing mononuclear phagocytes. Provided the antigen is cleared and the immune system of the host is fully functional, the acute inflammatory response will resolve. Until now it is considered that resolution then leads back to homeostasis, the physiological state tissues experienced before inflammation occurred. Using a human model of acute inflammation driven by intradermal UV killed Escherichia coli, we found that bacteria and granulocyte clearance as well as pro-inflammatory cytokine catabolism occurred by 72h. However, following a lag phase of about 4 days there was an increase in numbers of memory T cells and CD163+ macrophage at the post-resolution site up to day 17 as well as increased biosynthesis of cyclooxygenase-derived prostanoids and DHA-derived D series resolvins. Inhibiting post-resolution prostanoids using naproxen showed that numbers of tissue memory CD4 cells were under the endogenous control of PGE2, which exerts its suppressive effects on T cell proliferation via the EP4 receptor. In addition, we re-challenged the post-resolution site with a second injection of E. coli, which when compared to saline controls resulted in primarily a macrophage-driven response with comparatively fewer PMNs; the macrophage-dominated response was reversed by cyclooxygenase inhibition. Re-challenge experiments were also carried out in mice where we obtained similar results as in humans. Therefore, we report that acute inflammatory responses in both humans and rodents do not revert back to homeostasis, but trigger a hitherto unappreciated sequence of immunological events that dictate subsequent immune response to infection.

Indexed as

Acute DiseaseAdultAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenCell CountCell ProliferationDinoprostoneEscherichia coliFemaleHumansInflammationMacrophagesMaleMiceAntigens, CDAntigens, Differentiation, MyelomonocyticCD163 AntigenDinoprostoneReceptors, Cell Surface

Identifiers

PMID29073216
PMCPMC5658111
OpenAlexW2766972771

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.