Evidence map›Paper›PMID 29730187›Full record

ArticleJournal of clinical lipidology

Identification of proresolving and inflammatory lipid mediators in human psoriasis.

Alexander V Sorokin, Paul C Norris, Justin T English, Amit K Dey, Abhishek Chaturvedi, Yvonne Baumer, Joanna Silverman, Martin P Playford, Charles N Serhan, Nehal N Mehta

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical lipidology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 51 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Alexander V SorokinSection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Paul C NorrisCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative, and Pain Medicine, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Justin T EnglishCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative, and Pain Medicine, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Amit K DeySection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Abhishek ChaturvediSection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Yvonne BaumerSection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Joanna SilvermanSection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Martin P PlayfordSection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Charles N SerhanCenter for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative, and Pain Medicine, Harvard Institutes of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Nehal N MehtaSection of Inflammation and Cardiometabolic Diseases, Cardio-Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: nehal.mehta@nih.gov.
National Institutes of Health · USBrigham and Women's Hospital · US

Funding

Human Translational Studies of Inflammation and Cardiometabolic Diseases: The Psoriasis, Atherosclerosis and Cardiometabolic disease (PACI) InitiativeZIAHL006193 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2014 to 2023
$25.0M
Resolution Mechanisms in Acute Inflammation: Resolution PharmacologyP01GM095467 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI PETASIS, NICOS A · 2011 to 2020
$14.8M
In-vitro and Pre-clinical Translational Studies of Inflammation and AtherosclerosisZIAHL006235 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SACK, MICHAEL · 2018 to 2023
$6.7M
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
Intramural NIH HHS ZIA HL006193NIGMS NIH HHS P01 GM095467NIGMS NIH HHS R01 GM038765NIGMS NIH HHS R37 GM038765
6 · The paper itself

Abstract

backgroundPsoriasis (PSO) is an immune-mediated inflammatory disease associated with metabolic and cardiovascular comorbidities. It is now known that resolution of inflammation is an active process locally controlled by specialized proresolving mediators (SPMs), named resolvins (Rvs), protectins, and maresins.

objectiveIt is unknown whether these potent lipid mediators (LMs) are involved in PSO pathophysiology and if the skin and blood have disease-specific SPMs phenotype profiles.

methodsWe used liquid chromatography-tandem mass spectrometry-based LM metabololipidomics to obtain skin and peripheral blood LM profiles from PSO compared to healthy subjects. Some LMs were tested in cell culture experiments with corresponding gene expression and protein concentration analyses.

resultsThe levels of several LM were significantly elevated in lesional PSO skin compared to nonlesional and skin from healthy subjects. Particularly, RvD5, protectins Dx, and aspirin-triggered forms of lipoxin were present only in lesional PSO skin, whereas protectin D1 was present in nonlesional PSO skin. To determine specific roles of SPMs on skin-related inflammatory cytokines, RvD1 and RvD5 were incubated with human keratinocytes. RvD1 and RvD5 reduced the expression levels of interleukin 24 and S100A12, whereas only RvD1 significantly abrogated interleukin-24 production by keratinocytes.

conclusionsThese findings suggest that an imbalance between locally produced proresolution and proinflammatory LMs identified in PSO skin and blood compartments might play a role in PSO pathophysiology. Moreover, some of the PSO-related cytokines can be modified by specific SPMs and involved mechanisms support investigation of targeting novel proresolving lipid mediators as a therapy for PSO.

Indexed as

AdultAgedCase-Control StudiesCytokinesDocosahexaenoic AcidsFemaleHumansInflammation MediatorsInterleukin-24InterleukinsKeratinocytesLipidsLipoxinsMaleMiddle AgedPsoriasisCytokinesDocosahexaenoic AcidsInflammation MediatorsInterleukin-24InterleukinsLipidsLipoxinsprotectin D1resolvin D1resolvin D5S100A12 ProteinDHAEssential polyunsaturated fatty acidsInflammationLipid mediatorsPsoriasisResolution

Identifiers

PMID29730187
PMCPMC6112609
OpenAlexW2796355296

What OpenQuestion holds

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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.