Evidence map›Paper›PMID 24045576›Full record

ArticleMucosal immunology2014

Tumor necrosis factor-related apoptosis-inducing ligand translates neonatal respiratory infection into chronic lung disease.

M R Starkey, D H Nguyen, A T Essilfie, R Y Kim, L M Hatchwell, A M Collison, H Yagita, P S Foster, J C Horvat, J Mattes and 1 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2014. 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
1.5field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Asthma-COPD overlap: current understanding and the utility of experimental models.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  8. Cellular mechanisms underlying steroid-resistant asthma.European respiratory review : an official journal of the European Respiratory Society · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Divergent Roles for TRAIL in Lung Diseases.Frontiers in medicine · 2018
    Review
  14. Modeling TImmunological reviews · 2017
    Review
  15. Article
  16. Microbiome effects on immunity, health and disease in the lung.Clinical & translational immunology · 2017
    Review
  17. Article
  18. Review
  19. Article
  20. 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

11 authors at 3 institutions in 3 countries.

M R StarkeyPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
D H NguyenPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
A T EssilfiePriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
R Y KimPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
L M HatchwellPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
A M CollisonPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
H YagitaDepartment of Immunology, Juntendo University School of Medicine, Hongo, Bunkyo-ku, Tokyo, Japan.
P S FosterPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
J C HorvatPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
J Mattes1] Priority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia [2] Pediatric Respiratory and Sleep Medicine Unit, Newcastle Children's Hospital, Kaleidoscope, New Lambton Heights, Newcastle, New South Wales, Australia.
P M HansbroPriority Research Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Newcastle, New South Wales, Australia.
Hunter Medical Research Institute · AUBoston Children's Hospital · USJuntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Respiratory infections in early life can lead to chronic respiratory disease. Chlamydia infections are common causes of respiratory disease, particularly pneumonia in neonates, and are linked to permanent reductions in pulmonary function and the induction of asthma. However, the immune responses that protect against early-life infection and the mechanisms that lead to chronic lung disease are incompletely understood. Here we identify novel roles for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in promoting Chlamydia respiratory infection-induced pathology in early life, and subsequent chronic lung disease. By infecting TRAIL-deficient neonatal mice and using neutralizing antibodies against this factor and its receptors in wild-type mice, we demonstrate that TRAIL is critical in promoting infection-induced histopathology, inflammation, and mucus hypersecretion, as well as subsequent alveolar enlargement and impaired lung function. This suggests that therapeutic agents that target TRAIL or its receptors may be effective treatments for early-life respiratory infections and associated chronic lung disease.

Indexed as

AnimalsAnimals, NewbornAntibodies, NeutralizingApoptosisChlamydia InfectionsChlamydia muridarumDisease Models, AnimalDisease ProgressionGene ExpressionMiceMice, KnockoutMucusNF-kappa BPneumoniaPulmonary AlveoliReceptors, TNF-Related Apoptosis-Inducing LigandAntibodies, NeutralizingNF-kappa BReceptors, TNF-Related Apoptosis-Inducing LigandTNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID24045576
OpenAlexW1967376415

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.