Evidence map›Paper›PMID 27115946›Full record

ArticleAnnals of the American Thoracic Society2016

Neutrophil Fates in Bronchiectasis and Alpha-1 Antitrypsin Deficiency.

Derek W Russell, Amit Gaggar, George M Solomon

Abstract read
In one paragraph

Article in Annals of the American Thoracic Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  8. Article
  9. Extracellular vesicles and COPD: foe or friend?Journal of nanobiotechnology · 2023
    Review
  10. Article
  11. Article
  12. Foods (Basel, Switzerland) · 2021
    Article
  13. Article
  14. TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin.American journal of physiology. Cell physiology · 2020
    Article
  15. CFTR targeted therapies: recent advances in cystic fibrosis and possibilities in other diseases of the airways.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  16. Dissociation of systemic and mucosal autoimmunity in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020
    Article
  17. Article
  18. Article
  19. Review
  20. High prevalence of bronchiectasis in emphysema-predominant COPD patients.International journal of chronic obstructive pulmonary disease · 2018
    Article
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

3 authors.

Derek W Russell1 Department of Medicine.
Amit Gaggar1 Department of Medicine.
George M Solomon1 Department of Medicine.

Funding

A Novel Proteolytic System of Pulmonary InflammationR01HL102371 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GAGGAR, AMIT · 2010 to 2021
$3.3M
Genetics of Smoke-Altered LTA4H in COPDR01HL126596 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BLALOCK, J EDWIN, CASTALDI, PETER · 2015 to 2018
$1.6M
Prolyl Endopeptidase-Mediated Matrix Remodeling and Inflammation in COPDI01BX001756 · VA · BIRMINGHAM VA MEDICAL CENTER · PI GAGGAR, AMIT · 2015 to 2018
–
BLRD VA I01 BX001756NHLBI NIH HHS R01 HL102371NHLBI NIH HHS R01 HL126596
6 · The paper itself

Abstract

The neutrophil is a powerful cellular defender of the vulnerable interface between the environment and pulmonary tissues. This cell's potent weapons are carefully calibrated in the healthy state to maximize effectiveness in fighting pathogens while minimizing tissue damage and allowing for repair of what damage does occur. The three related chronic airway disorders of cystic fibrosis, non-cystic fibrosis bronchiectasis, and alpha-1 antitrypsin deficiency all demonstrate significant derangements of this homeostatic system that result in their respective pathologies. An important shared feature among them is the inefficient resolution of chronic inflammation that serves as a central means for neutrophil-driven lung damage resulting in disease progression. Examining the commonalities and divergences between these diseases in the light of their immunopathology is informative and may help guide us toward future therapeutics designed to modulate the neutrophil's interplay with the pulmonary environment.

Indexed as

alpha 1-Antitrypsin DeficiencyBronchiectasisCystic FibrosisDisease ProgressionHumansLungNeutrophilsalpha-1 antitrypsin deficiencybronchiectasiscystic fibrosisneutrophilneutrophil elastase

Identifiers

PMID27115946
PMCPMC5015725

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.