Evidence map›Paper›PMID 22878412›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Prolonged injury and altered lung function after ozone inhalation in mice with chronic lung inflammation.

Angela M Groves, Andrew J Gow, Christopher B Massa, Jeffrey D Laskin, Debra L Laskin

Abstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Inhaled ozone induces distinct alterations in pulmonary function in models of acute and episodic exposure in female mice.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Role of PPARγ in dyslipidemia and altered pulmonary functioning in mice following ozone exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  7. Article
  8. Review
  9. Regulation of Lung Macrophage Activation and Oxidative Stress Following Ozone Exposure by Farnesoid X Receptor.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  10. Review
  11. Article
  12. Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  13. Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Review
  14. Review
  15. Protective Role of Surfactant Protein-D Against Lung Injury and Oxidative Stress Induced by Nitrogen Mustard.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
  16. Review
  17. Article
  18. Article
  19. Editor's Highlight: Role of Spleen-Derived Macrophages in Ozone-Induced Lung Inflammation and Injury.Toxicological sciences : an official journal of the Society of Toxicology · 2017
    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

5 authors at 1 institution in 1 country.

Angela M GrovesDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854, USA.
Andrew J Gow
Christopher B Massa
Jeffrey D Laskin
Debra L Laskin
Rutgers, The State University of New Jersey · US

Funding

UMDNJ/Rutgers University CounterACT Research Center of ExcellenceU54AR055073 · NIAMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI HECK, DIANE E · 2006 to 2024
$71.4M
Translational Research Support CoreP30ES005022 · NIEHS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI ROBERT John LAUMBACH · 1988 to 2026
$47.4M
TRAINING IN EVIRONMENTAL TOXICOLOGYT32ES007148 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Lauren M Aleksunes · 1987 to 2026
$11.4M
ACTIVATED MACROPHAGES AND OZONE TOXICITYR01ES004738 · NIEHS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI Debra L Laskin · 1989 to 2026
$9.0M
ROLE OF KUPFFER CELLS IN CHEMICAL TOXICITYR01GM034310 · NIGMS · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI LASKIN, DEBRA L · 1985 to 2009
$3.1M
NO-Modified Biomolecules and Pulmonary SignalingR01HL086621 · NHLBI · RUTGERS, THE STATE UNIV OF N.J. · PI GOW, ANDREW J · 2008 to 2016
$2.8M
Macrophages and Inflammatory Mediators in Silica-Induced CarcinogenesisR01CA132624 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI LASKIN, DEBRA L · 2008 to 2012
$1.5M
NCI NIH HHS R01 CA132624NCI NIH HHS R01CA132624NHLBI NIH HHS R01 HL086621NHLBI NIH HHS R01HL086621NIAMS NIH HHS U54 AR055073NIAMS NIH HHS U54AR055073NIEHS NIH HHS P30 ES005022NIEHS NIH HHS P30ES005022NIEHS NIH HHS R01 ES004738NIEHS NIH HHS R01ES004738NIEHS NIH HHS T32 ES007148NIEHS NIH HHS T32ES007148NIGMS NIH HHS R01 GM034310NIGMS NIH HHS R01GM034310
6 · The paper itself

Abstract

Surfactant protein-D (Sftpd) is a pulmonary collectin important in down-regulating macrophage inflammatory responses. In these experiments, we analyzed the effects of chronic macrophage inflammation attributable to loss of Sftpd on the persistence of ozone-induced injury, macrophage activation, and altered functioning in the lung. Wild-type (Sftpd(+/+)) and Sftpd(-/-) mice (aged 8 wk) were exposed to air or ozone (0.8 parts per million, 3 h). Bronchoalveolar lavage (BAL) fluid and tissue were collected 72 hours later. In Sftpd(-/-) mice, but not Sftpd(+/+) mice, increased BAL protein and nitrogen oxides were observed after ozone inhalation, indicating prolonged lung injury and oxidative stress. Increased numbers of macrophages were also present in BAL fluid and in histologic sections from Sftpd(-/-) mice. These cells were enlarged and foamy, suggesting that they were activated. This conclusion was supported by findings of increased BAL chemotactic activity, and increased expression of inducible nitric oxide synthase in lung macrophages. In both Sftpd(+/+) and Sftpd(-/-) mice, inhalation of ozone was associated with functional alterations in the lung. Although these alterations were limited to central airway mechanics in Sftpd(+/+) mice, both central airway and parenchymal mechanics were modified by ozone exposure in Sftpd(-/-) mice. The most notable changes were evident in resistance and elastance spectra and baseline lung function, and in lung responsiveness to changes in positive end-expiratory pressure. These data demonstrate that a loss of Sftpd is associated with prolonged lung injury, oxidative stress, and macrophage accumulation and activation in response to ozone, and with more extensive functional changes consistent with the loss of parenchymal integrity.

Indexed as

Air PollutantsAirway ResistanceAnimalsElasticityInhalation ExposureLungLung InjuryMacrophage ActivationMacrophages, AlveolarMaleMiceMice, Inbred C57BLMice, KnockoutNitric Oxide Synthase Type IINitrogen OxidesOzoneAir PollutantsNitric Oxide Synthase Type IINitrogen OxidesNos2 protein, mouseOzonePulmonary Surfactant-Associated Protein D

Identifiers

PMID22878412
PMCPMC3547091
OpenAlexW2091396999

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.