Evidence map›Paper›PMID 22727909›Full record

ArticleToxicology and applied pharmacology2012

Classical and alternative macrophage activation in the lung following ozone-induced oxidative stress.

Vasanthi R Sunil, Kinal Patel-Vayas, Jianliang Shen, Jeffrey D Laskin, Debra L Laskin

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Single-cell transcriptomics reveal alveolar macrophage-specific responses in single-hit ozone exposure model in mice.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article
  5. Article
  6. Evaluating the role of alveolar macrophages in tolerance to ozone.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  7. Review
  8. 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
  9. Article
  10. Article
  11. Article
  12. Article
  13. 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
  14. Aerosol physicochemical determinants of carbon black and ozone inhalation co-exposure induced pulmonary toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  15. Article
  16. Article
  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

5 authors at 1 institution in 1 country.

Vasanthi R SunilDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854, USA. sunilva@pharmacy.rutgers.edu
Kinal Patel-Vayas
Jianliang Shen
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
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
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 R01CA132624NIAMS NIH HHS U54 AR055073NIAMS NIH HHS U54AR055073NIEHS NIH HHS P30 ES005022NIEHS NIH HHS P30ES05022NIEHS NIH HHS R01 ES004738NIEHS NIH HHS R01ES004738NIGMS NIH HHS R01 GM034310NIGMS NIH HHS R01GM034310
6 · The paper itself

Abstract

Ozone is a pulmonary irritant known to cause oxidative stress, inflammation and tissue injury. Evidence suggests that macrophages play a role in the pathogenic response; however, their contribution depends on the mediators they encounter in the lung which dictate their function. In these studies we analyzed the effects of ozone-induced oxidative stress on the phenotype of alveolar macrophages (AM). Exposure of rats to ozone (2 ppm, 3h) resulted in increased expression of 8-hydroxy-2'-deoxyguanosine (8-OHdG), as well as heme oxygenase-1 (HO-1) in AM. Whereas 8-OHdG was maximum at 24h, expression of HO-1 was biphasic increasing after 3h and 48-72 h. Cleaved caspase-9 and beclin-1, markers of apoptosis and autophagy, were also induced in AM 24h post-ozone. This was associated with increased bronchoalveolar lavage protein and cells, as well as matrix metalloproteinase (MMP)-2 and MMP-9, demonstrating alveolar epithelial injury. Ozone intoxication resulted in biphasic activation of the transcription factor, NFκB. This correlated with expression of monocyte chemotactic protein-1, inducible nitric oxide synthase and cyclooxygenase-2, markers of proinflammatory macrophages. Increases in arginase-1, Ym1 and galectin-3 positive anti-inflammatory/wound repair macrophages were also observed in the lung after ozone inhalation, beginning at 24h (arginase-1, Ym1), and persisting for 72 h (galectin-3). This was associated with increased expression of pro-surfactant protein-C, a marker of Type II cell proliferation and activation, important steps in wound repair. These data suggest that both proinflammatory/cytotoxic and anti-inflammatory/wound repair macrophages are activated early in the response to ozone-induced oxidative stress and tissue injury.

Indexed as

8-Hydroxy-2'-DeoxyguanosineAnimalsApoptosisAutophagyCell ProliferationDeoxyguanosineFemaleGene Expression RegulationHeme Oxygenase-1InflammationLungMacrophages, AlveolarOxidative StressOzoneProtein CRats8-Hydroxy-2'-DeoxyguanosineDeoxyguanosineHeme Oxygenase-1OzoneProtein C

Identifiers

PMID22727909
PMCPMC3670689
OpenAlexW2078144779

What OpenQuestion holds

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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.