Evidence map›Paper›PMID 28596972›Full record

ReviewJournal of immunology research2017

Targets of Neutrophil Influx and Weaponry: Therapeutic Opportunities for Chronic Obstructive Airway Disease.

Carina Kärrman Mårdh, James Root, Mohib Uddin, Kristina Stenvall, Anna Malmgren, Kostas Karabelas, Matthew Thomas

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The roles of neutrophils in non-tuberculous mycobacterial pulmonary disease.Annals of clinical microbiology and antimicrobials · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Neutrophils as emerging therapeutic targets.Nature reviews. Drug discovery · 2020
    Review
  12. Article
  13. Article
  14. Role of Inflammatory Cell Subtypes in Heart Failure.Journal of immunology research · 2019
    Review
  15. Review
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

7 authors at 1 institution in 1 country.

Carina Kärrman MårdhRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.ORCID 0000-0001-5644-9294
James RootRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.
Mohib UddinRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.
Kristina StenvallRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.
Anna MalmgrenRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.
Kostas KarabelasRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.
Matthew ThomasRespiratory, Inflammation and Autoimmunity IMED, AstraZeneca R&D, Gothenburg, Sweden.
AstraZeneca (Sweden) · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils are important effector cells of antimicrobial immunity in an acute inflammatory response, with a primary role in the clearance of extracellular pathogens. However, in respiratory diseases such as asthma and chronic obstructive pulmonary disease (COPD), there is excessive infiltration and activation of neutrophils, subsequent production of reactive oxygen species, and release of serine proteases, matrix metalloproteinases, and myeloperoxidase-resulting in collateral damage as the cells infiltrate into the tissue. Increased neutrophil survival through dysregulated apoptosis facilitates continued release of neutrophil-derived mediators to perpetuate airway inflammation and tissue injury. Several target mechanisms have been investigated to address pathologic neutrophil biology and thereby provide a novel therapy for respiratory disease. These include neutrophil influx through inhibition of chemokine receptors CXCR2, CXCR1, and PI3K

Indexed as

AnimalsAnti-Inflammatory AgentsAsthmaCell MovementHumansInflammation MediatorsNeutrophilsPhosphoinositide-3 Kinase InhibitorsPulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesReceptors, Interleukin-8AReceptors, Interleukin-8BRespiratory SystemSignal TransductionAnti-Inflammatory AgentsInflammation MediatorsPhosphoinositide-3 Kinase InhibitorsReactive Oxygen SpeciesReceptors, Interleukin-8AReceptors, Interleukin-8B

Identifiers

PMID28596972
PMCPMC5449733
OpenAlexW2615682155

What OpenQuestion holds

Textmetadata
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.