Evidence map›Paper›PMID 25724551›Full record

ArticleToxicology and applied pharmacology2015

Regulation of ozone-induced lung inflammation and injury by the β-galactoside-binding lectin galectin-3.

Vasanthi R Sunil, Mary Francis, Kinal N Vayas, Jessica A Cervelli, Hyejeong Choi, Jeffrey D Laskin, Debra L Laskin

Abstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Article
  3. 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
  4. Article
  5. Review
  6. Article
  7. Article
  8. 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
  9. Article
  10. Article
  11. Article
  12. Microvesicle-Derived miRNAs Regulate Proinflammatory Macrophage Activation in the Lung Following Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2022
    Article
  13. Article
  14. 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
  15. Article
  16. Review
  17. Article
  18. Transcriptional Profiling of the Murine Airway Response to Acute Ozone Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  19. Sex Modifies Acute Ozone-Mediated Airway Physiologic Responses.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  20. 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
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

7 authors at 2 institutions in 1 country.

Vasanthi R SunilDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ, United States. Electronic address: sunilva@pharmacy.rutgers.edu.
Mary FrancisDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ, United States. Electronic address: maryfranrutgers@gmail.com.
Kinal N VayasDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ, United States. Electronic address: kinalv5@gmail.com.
Jessica A CervelliDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ, United States. Electronic address: j.cervelli@pharmacy.rutgers.edu.
Hyejeong ChoiDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ, United States. Electronic address: choi@eohsi.rutgers.edu.
Jeffrey D LaskinDepartment of Environmental and Occupational Medicine, Rutgers University, Robert Wood Johnson Medical School, Piscataway, NJ, United States. Electronic address: jlaskin@eohsi.rutgers.edu.
Debra L LaskinDepartment of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ, United States. Electronic address: laskin@eohsi.rutgers.edu.
Rutgers, The State University of New Jersey · USJohnson University · 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
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 CA132624NIAMS NIH HHS AR055073NIAMS NIH HHS U54 AR055073NIEHS NIH HHS ES004738NIEHS NIH HHS ES005022NIEHS NIH HHS ES007148NIEHS NIH HHS P30 ES005022NIEHS NIH HHS R01 ES004738NIEHS NIH HHS T32 ES007148
6 · The paper itself

Abstract

Macrophages play a dual role in ozone toxicity, contributing to both pro- and anti-inflammatory processes. Galectin-3 (Gal-3) is a lectin known to regulate macrophage activity. Herein, we analyzed the role of Gal-3 in the response of lung macrophages to ozone. Bronchoalveolar lavage (BAL) and lung tissue were collected 24-72h after exposure (3h) of WT and Gal-3(-/-) mice to air or 0.8ppm ozone. In WT mice, ozone inhalation resulted in increased numbers of proinflammatory (Gal-3(+), iNOS(+)) and anti-inflammatory (MR-1(+)) macrophages in the lungs. While accumulation of iNOS(+) macrophages was attenuated in Gal-3(-/-) mice, increased numbers of enlarged MR-1(+) macrophages were noted. This correlated with increased numbers of macrophages in BAL. Flow cytometric analysis showed that these cells were CD11b(+) and consisted mainly (>97%) of mature (F4/80(+)CD11c(+)) proinflammatory (Ly6GLy6C(hi)) and anti-inflammatory (Ly6GLy6C(lo)) macrophages. Increases in both macrophage subpopulations were observed following ozone inhalation. Loss of Gal-3 resulted in a decrease in Ly6C(hi) macrophages, with no effect on Ly6C(lo) macrophages. CD11b(+)Ly6G(+)Ly6C(+) granulocytic (G) and monocytic (M) myeloid derived suppressor cells (MDSC) were also identified in the lung after ozone. In Gal-3(-/-) mice, the response of G-MDSC to ozone was attenuated, while the response of M-MDSC was heightened. Changes in inflammatory cell populations in the lung of ozone treated Gal-3(-/-) mice were correlated with reduced tissue injury as measured by cytochrome b5 expression. These data demonstrate that Gal-3 plays a role in promoting proinflammatory macrophage accumulation and toxicity in the lung following ozone exposure.

Indexed as

AnimalsFemaleGalactosidesGalectin 3GalectinsLungLung InjuryMacrophages, AlveolarMiceMice, Inbred C57BLNitric Oxide Synthase Type IIOzonePneumoniabeta-galactosideGalactosidesGalectin 3GalectinsNitric Oxide Synthase Type IINos2 protein, mouseOzoneFlow cytometryGal-3Macrophage phenotypeMDSCOzone

Identifiers

PMID25724551
PMCPMC4408237
OpenAlexW2011536415

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.