Evidence map›Paper›PMID 30089723›Full record

ArticleJCI insight2018

IL-16/miR-125a axis controls neutrophil recruitment in pristane-induced lung inflammation.

Siobhan Smith, Pei Wen Wu, Jane J Seo, Thilini Fernando, Mengyao Jin, Jorge Contreras, Erica N Montano, Joan Ní Gabhann, Kyle Cunningham, Amro Widaa and 13 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. 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
2.8field-weighted citation impact, top 9% 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, 47 citations in OpenAlex.

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  9. Emerging microbes & infections · 2024
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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

23 authors at 7 institutions in 4 countries.

Siobhan SmithDepartment of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Pei Wen WuDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Jane J SeoDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Thilini FernandoDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Mengyao JinDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Jorge ContrerasDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Erica N MontanoDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Joan Ní GabhannDepartment of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Kyle CunninghamDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Amro WidaaDepartment of Anatomy, Royal College of Surgeons in Ireland, Dublin, Ireland.
Eoghan M McCarthyDepartment of Rheumatology, Beaumont Hospital, Dublin, Ireland.
Eamonn S MolloyDepartment of Rheumatology, St. Vincent's University Hospital, Dublin, Ireland.
Grainne KearnsDepartment of Rheumatology, Beaumont Hospital, Dublin, Ireland.
Conor C MurphyDepartment of Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland.
Weiping KongChina-Japan Friendship Hospital, Chaoyang District, Beijing, China.
Harry BjörkbackaExperimental Cardiovascular Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden.
Hardy KornfeldDepartment of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Lindsy ForbessDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Swamy VenuturupalliDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Mariko IshimoriDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Daniel WallaceDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Michael H WeismanDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Caroline A JefferiesDivision of Rheumatology, Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Cedars-Sinai Medical Center · USRoyal College of Surgeons in Ireland · IEBeaumont Hospital · IEChina-Japan Friendship Hospital · CNLund University · SESt. Vincent's University Hospital · IEUniversity of Massachusetts Chan Medical School · US

Funding

Determinants of Tuberculosis SeverityR01HL127384 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KORNFELD, HARDY · 2016 to 2019
$2.2M
NHLBI NIH HHS R01 HL127384
6 · The paper itself

Abstract

Severe lung inflammation and alveolar hemorrhage can be life-threatening in systemic lupus erythematosus (SLE) patients if not treated early and aggressively. Neutrophil influx is the driver key of this pathology, but little is known regarding the molecular events regulating this recruitment. Here, we uncover a role for IL-16/mir-125a in this pathology and show not only that IL-16 is a target for miR-125a but that reduced miR-125a expression in SLE patients associates with lung involvement. Furthermore, in the pristane model of acute "SLE-like" lung inflammation and alveolar hemorrhage, we observed reduced pulmonary miR-125a and enhanced IL-16 expression. Neutrophil infiltration was markedly reduced in the peritoneal lavage of pristane-treated IL-16-deficient mice and elevated following i.n. delivery of IL-16. Moreover, a miR-125a mimic reduced pristane-induced IL-16 expression and neutrophil recruitment and rescued lung pathology. Mechanistically, IL-16 acts directly on the pulmonary epithelium and markedly enhances neutrophil chemoattractant expression both in vitro and in vivo, while the miR-125a mimic can prevent this. Our results reveal a role for miR-125a/IL-16 in regulating lung inflammation and suggest this axis may be a therapeutic target for management of acute lung injury in SLE.

Indexed as

AdultAnimalsCell LineDisease Models, AnimalEpitheliumFemaleGene Expression RegulationHumansInterleukin-16LungLupus Erythematosus, SystemicMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutIl16 protein, humanIl16 protein, mouseInterleukin-16MicroRNAsMIRN125 microRNA, humanMirn125 microRNA, mousepristaneTerpenesAutoimmunityChemokinesImmunologyLupusNeutrophils

Identifiers

PMID30089723
PMCPMC6129123
OpenAlexW2886766736

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.