Evidence map›Paper›PMID 30696002›Full record

ArticleInternational journal of molecular sciences2019

The Cutaneous Inflammatory Response to Thermal Burn Injury in a Murine Model.

Zabeen Lateef, Gabriella Stuart, Nicola Jones, Andrew Mercer, Stephen Fleming, Lyn Wise

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

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  16. Alginate and Nanocellulose Dressings With Extract From Salmon Roe Reduce Inflammation and Accelerate Healing of Porcine Burn Wounds.Journal of burn care & research : official publication of the American Burn Association · 2023
    Article
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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

6 authors.

Zabeen LateefDepartment of Pharmacology and Toxicology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. zabeen.lateef@otago.ac.nz.ORCID 0000-0001-5987-7665
Gabriella StuartDepartment of Pharmacology and Toxicology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. gabriella.stuart@otago.ac.nz.
Nicola JonesDepartment of Pharmacology and Toxicology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. nicky.jones@otago.ac.nz.
Andrew MercerDepartment of Microbiology and Immunology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. andy.mercer@otago.ac.nz.
Stephen FlemingDepartment of Microbiology and Immunology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. stephen.fleming@otago.ac.nz.
Lyn WiseDepartment of Pharmacology and Toxicology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. lyn.wise@otago.ac.nz.ORCID 0000-0003-0646-8424

Funding

Health Research Council of New Zealand 13/774
6 · The paper itself

Abstract

Many burn interventions aim to target the inflammatory response as a means of enhancing healing or limiting hypertrophic scarring. Murine models of human burns have been developed, but the inflammatory response to injury in these models has not been well defined. The aim of this study was to profile inflammatory cell populations and gene expression relative to healing and scarring in a murine model of thermal burns. Cutaneous injuries were created on the dorsal region of C57Bl/6 mice using a heated metal rod. Animals were euthanized at selected time points over ten weeks, with the lesions evaluated using macroscopic measurements, histology, immunofluorescent histochemistry and quantitative PCR. The burn method generated a reproducible, partial-thickness injury that healed within two weeks through both contraction and re-epithelialization, in a manner similar to human burns. The injury caused an immediate increase in pro-inflammatory cytokine and chemokine expression, coinciding with an influx of neutrophils, and the disappearance of Langerhans cells and mast cells. This preceded an influx of dendritic cells and macrophages, a quarter of which displayed an inflammatory (M1) phenotype, with both populations peaking at closure. As with human burns, the residual scar increased in size, epidermal and dermal thickness, and mast cell numbers over 10 weeks, but abnormal collagen I-collagen III ratios, fibre organization and macrophage populations resolved 3⁻4 weeks after closure. Characterisation of the inflammatory response in this promising murine burn model will assist future studies of burn complications and aid in the preclinical testing of new anti-inflammatory and anti-scarring therapies.

Indexed as

Hot TemperatureAnimalsBurnsCicatrixDisease Models, AnimalFemaleFibrosisGene Expression RegulationInflammationMice, Inbred C57BLRe-EpithelializationSkincollagendendritic cellhypertrophic scarinflammationLangerhans cellmacrophagemast cellmiceneutrophilthermal burn

Identifiers

PMID30696002
PMCPMC6387172

What OpenQuestion holds

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LicenceCC BY
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.