Evidence map›Paper›PMID 23258231›Full record

ArticleAmerican journal of respiratory cell and molecular biology2013

Neonatal hyperoxia increases sensitivity of adult mice to bleomycin-induced lung fibrosis.

Min Yee, Bradley W Buczynski, B Paige Lawrence, Michael A O'Reilly

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Low-dose hyperoxia primes airways for fibrosis in mice after influenza A infection.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Early origins of lung disease: towards an interdisciplinary approach.European respiratory review : an official journal of the European Respiratory Society · 2020
    Review
  9. Myeloid-derived Suppressor Cells Are Necessary for Development of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Neonatal hyperoxia stimulates the expansion of alveolar epithelial type II cells.American journal of respiratory cell and molecular biology · 2014
    Article
  15. Review
  16. Neonatal hyperoxia alters the host response to influenza A virus infection in adult mice through multiple pathways.American journal of physiology. Lung cellular and molecular physiology · 2013
    Article
  17. Bronchopulmonary dysplasia: what are its links to COPD?Therapeutic advances in respiratory disease
    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

4 authors at 2 institutions in 1 country.

Min YeeDepartment of Pediatrics, School of Medicine and Dentistry, University of Rochester, Rochester, NY 14642, USA.
Bradley W Buczynski
B Paige Lawrence
Michael A O'Reilly
Pediatrics and Genetics · USUniversity of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Sally W Thurston · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
MULTIDISCIPLINARY TRAINING IN PULMONARY RESEARCHT32HL066988 · NHLBI · UNIVERSITY OF ROCHESTER · PI GEORAS, STEVE N, O'REILLY, MICHAEL A · 2001 to 2021
$8.1M
Effect of Neonatal Hyperoxia on Alveolar Development and InfectionR01HL091968 · NHLBI · UNIVERSITY OF ROCHESTER · PI O'REILLY, MICHAEL A · 2009 to 2021
$5.4M
Neonatal Oxygen and Susceptibility to Respiratory Viral InfectionsR01HL097141 · NHLBI · UNIVERSITY OF ROCHESTER · PI LAWRENCE, B PAIGE, O'REILLY, MICHAEL A · 2009 to 2013
$2.5M
Environmental Influences on Epigenetic Immune ProgrammingR01ES017250 · NIEHS · UNIVERSITY OF ROCHESTER · PI LAWRENCE, B PAIGE · 2011 to 2015
$1.8M
BCL-2, ROS, AND CELL DEATH IN DEVELOPMENTAL TOXICITYR01ES007026 · NIEHS · UNIVERSITY OF WASHINGTON · PI MIRKES, PHILIP E · 1996 to 2002
$1.2M
NHLBI NIH HHS HL-091968NHLBI NIH HHS HL-097141NHLBI NIH HHS HL-66988NHLBI NIH HHS R01 HL091968NHLBI NIH HHS R01 HL097141NHLBI NIH HHS T32 HL066988NIEHS NIH HHS ES-01247NIEHS NIH HHS ES-017250NIEHS NIH HHS ES-07026NIEHS NIH HHS P30 ES001247NIEHS NIH HHS R01 ES007026NIEHS NIH HHS R01 ES017250NIEHS NIH HHS T32 ES007026
6 · The paper itself

Abstract

Supplemental oxygen used to treat infants born prematurely constitutes a major risk factor for long-term deficits in lung function and host defense against respiratory infections. Likewise, neonatal oxygen exposure results in alveolar simplification in adult mice, and enhances leukocyte recruitment and fibrosis when adult mice are infected with a sublethal dose of influenza A virus. Because pulmonary fibrosis was not observed in infected adult mice exposed to room air as neonates, previous neonatal oxygen exposure may have reprogrammed how the adult lung responds to epithelial injury. By administering bleomycin to adult mice exposed to room air or hyperoxia as neonates, we tested the hypothesis that neonatal hyperoxia enhances fibrosis when the epithelium is injured by direct fibrotic stimulus. Increased sensitivity to bleomycin-induced lung fibrosis was observed in adult mice exposed to neonatal hyperoxia, and was associated with increased numbers of leukocytes and an accumulation of active transforming growth factor (TGF)-β1 in the lung. Fate mapping of the respiratory epithelium revealed that the epithelial-mesenchymal transition was not a significant source of fibroblasts in room air-exposed or oxygen-exposed mice treated with bleomycin. Instead, the treatment of mice with anti-Gr-1 antibody that depletes neutrophils and myeloid-derived suppressor cells reduced the early activation of TGF-β1 and attenuated hyperoxia-enhanced fibrosis. Because bleomycin and influenza A virus both cause epithelial injury, understanding how neonatal hyperoxia reprograms the epithelial response to these two different injurious agents could lead to new therapeutic opportunities for treating lung diseases attributed to prematurity.

Indexed as

Animals, NewbornAnimalsBase SequenceDNA PrimersHyperoxiaImmunohistochemistryMicePulmonary FibrosisReal-Time Polymerase Chain ReactionDNA Primers

Identifiers

PMID23258231
PMCPMC3604066
OpenAlexW2052688459

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.