Evidence map›Paper›PMID 24862346›Full record

ArticleJournal of innate immunity2014

Cystic fibrosis sputum DNA has NETosis characteristics and neutrophil extracellular trap release is regulated by macrophage migration-inhibitory factor.

Markryan Dwyer, Qiang Shan, Samantha D'Ortona, Rie Maurer, Robert Mitchell, Hanne Olesen, Steffen Thiel, Johannes Huebner, Mihaela Gadjeva

Open access · bronzeAbstract read
In one paragraph

Article in Journal of innate immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

136 citing papers in PubMed, 1 synthesis or guideline pooled it, 207 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Neutrophil extracellular traps (NETosis) in gynecologic cancers: from pathogenesis to therapeutic opportunities: a narrative review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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76 more citing papers are in PubMed but not listed here.

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

9 authors at 5 institutions in 3 countries.

Markryan DwyerDepartment of Medicine, Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass., USA.
Qiang Shan
Samantha D'Ortona
Rie Maurer
Robert Mitchell
Hanne Olesen
Steffen Thiel
Johannes Huebner
Mihaela Gadjeva
Brigham and Women's Hospital · USAarhus University · DKAarhus University Hospital · DKLudwig-Maximilians-Universität München · DEUniversity of Louisville · US

Funding

Novel treatment strategies to regulate inflammation during P.aeruginosa keratitisR01EY022054 · NEI · BRIGHAM AND WOMEN'S HOSPITAL · PI GADJEVA, MIHAELA GUEORGUIEVA · 2012 to 2020
$4.0M
Role of MIF in Rb inactivation and TumorigenesisR01CA102285 · NCI · UNIVERSITY OF LOUISVILLE · PI MITCHELL, ROBERT A · 2004 to 2009
$1.4M
NCI NIH HHS R01 CA102285NEI NIH HHS R01 EY022054
6 · The paper itself

Abstract

Neutrophils are the main proinflammatory cell type in chronically infected lungs of cystic fibrosis (CF) patients; however, they fail to effectively clear the colonizing pathogens. Here, we investigated the molecular composition of non-mucoid and mucoid Pseudomonas aeruginosa-induced neutrophil extracellular traps (NETs) in vitro and compared them to the DNA-protein complexes present in the CF sputum. The protein composition of P. aeruginosa-induced NET fragments revealed that irrespective of the inducing stimuli, NET fragments were decorated with a conserved set of proteins. The DNA-protein complexes derived from CF sputum were consistent with NETosis and shared a similar protein signature, suggesting that the majority of the extracellular DNA was NET derived. The ability of polymorphonuclear leukocytes to produce NETs in response to P. aeruginosa was driven by macrophage migration-inhibitory factor (MIF) by promoting mitogen-activated protein kinase. Analysis of 132 CF patient samples revealed that elevated MIF protein levels correlated with poorer lung function. We suggest that targeting MIF by small molecular inhibitors might reduce the presence of extracellular DNA and serve as an adjunct to the use of antimicrobial drugs that could ultimately reduce bacterial fitness in the lungs during the later stages of CF disease.

Indexed as

AnimalsCystic FibrosisDNAExtracellular Signal-Regulated MAP KinasesExtracellular TrapsFemaleHumansIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMaleMiceMice, KnockoutPseudomonas aeruginosaSputumDNAExtracellular Signal-Regulated MAP KinasesIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMIF protein, humanMif protein, mouse

Identifiers

PMID24862346
PMCPMC4201867
OpenAlexW1968739991

What OpenQuestion holds

Textmetadata
LicenceTDM
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.