Evidence map›Paper›PMID 36359917›Full record

ReviewCells2022

Neutrophil Extracellular Traps in Asthma: Friends or Foes?

Remo Poto, Mohamed Shamji, Gianni Marone, Stephen R Durham, Guy W Scadding, Gilda Varricchi

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 39 citations in OpenAlex.

  1. Vascular remodeling in asthma: from mechanisms to precision medicine.Current opinion in allergy and clinical immunology · 2026
    Review
  2. Response to benralizumab in patients with severe eosinophilic asthma.Revista medica del Instituto Mexicano del Seguro Social · 2026
    Observational
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. NETosis in hypersensitivity disorders.Molecular biology reports · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 4 institutions in 2 countries.

Remo PotoDepartment of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0002-4723-0167
Mohamed ShamjiImmunomodulation and Tolerance Group, Allergy and Clinical Immunology, Inflammation, Repair, Development, National Heart and Lung Institute, Imperial College, London SW7 2AZ, UK.
Gianni MaroneDepartment of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0002-9849-4701
Stephen R DurhamAllergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK.
Guy W ScaddingAllergy and Clinical Immunology, National Heart and Lung Institute, Imperial College, London SW3 6LY, UK.
Gilda VarricchiDepartment of Translational Medical Sciences, University of Naples Federico II, 80131 Naples, Italy.ORCID 0000-0002-9285-4657
Imperial College London · GBInstitute for Experimental Endocrinology and Oncology · ITAsthma UK · GBWorld Health Organization - Italy · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma is a chronic inflammatory disease characterized by variable airflow limitation and airway hyperresponsiveness. A plethora of immune and structural cells are involved in asthma pathogenesis. The roles of neutrophils and their mediators in different asthma phenotypes are largely unknown. Neutrophil extracellular traps (NETs) are net-like structures composed of DNA scaffolds, histones and granular proteins released by activated neutrophils. NETs were originally described as a process to entrap and kill a variety of microorganisms. NET formation can be achieved through a cell-death process, termed NETosis, or in association with the release of DNA from viable neutrophils. NETs can also promote the resolution of inflammation by degrading cytokines and chemokines. NETs have been implicated in the pathogenesis of various non-infectious conditions, including autoimmunity, cancer and even allergic disorders. Putative surrogate NET biomarkers (e.g., double-strand DNA (dsDNA), myeloperoxidase-DNA (MPO-DNA), and citrullinated histone H3 (CitH3)) have been found in different sites/fluids of patients with asthma. Targeting NETs has been proposed as a therapeutic strategy in several diseases. However, different NETs and NET components may have alternate, even opposite, consequences on inflammation. Here we review recent findings emphasizing the pathogenic and therapeutic potential of NETs in asthma.

Indexed as

AsthmaExtracellular TrapsBiomarkersDNAHistonesHumansInflammationNeutrophilsBiomarkersDNAHistonesasthmainflammationNETsneutrophil extracellular trapsneutrophilsPMNTSLPVEGF

Identifiers

PMID36359917
PMCPMC9654069
OpenAlexW4308721283

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.