Evidence map›Paper›PMID 27240593›Full record

ArticleInhalation toxicology2016

Repeated ozone exposure exacerbates insulin resistance and activates innate immune response in genetically susceptible mice.

Jixin Zhong, Katryn Allen, Xiaoquan Rao, Zhekang Ying, Zachary Braunstein, Saumya R Kankanala, Chang Xia, Xiaoke Wang, Lori A Bramble, James G Wagner and 4 more

Open access · greenAbstract read
In one paragraph

Article in Inhalation toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Differential gene expression in nasal airway epithelium from overweight or obese youth with asthma.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2022
    Pooled it
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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

14 authors at 3 institutions in 1 country.

Jixin Zhonga Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
Katryn Allenb EPA Great Lakes Clean Air Research Center, Michigan State University , East Lansing , MI , USA .
Xiaoquan Raoa Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
Zhekang Yinga Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
Zachary Braunsteinc Boonshoft School of Medicine, Wright State University , Dayton , OH , USA , and.
Saumya R Kankanalaa Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
Chang Xiaa Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
Xiaoke Wanga Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
Lori A Brambleb EPA Great Lakes Clean Air Research Center, Michigan State University , East Lansing , MI , USA .
James G Wagnerb EPA Great Lakes Clean Air Research Center, Michigan State University , East Lansing , MI , USA .
Ryan Lewandowskib EPA Great Lakes Clean Air Research Center, Michigan State University , East Lansing , MI , USA .
Qinghua Sund Davis Heart & Lung Research Institute, Department of Internal Medicine, the Ohio State University , Columbus , OH , USA.
Jack R Harkemab EPA Great Lakes Clean Air Research Center, Michigan State University , East Lansing , MI , USA .
Sanjay Rajagopalana Division of Cardiovascular Medicine , Department of Medicine, University of Maryland School of Medicine , Baltimore , MD , USA .
University of Maryland, Baltimore · USMichigan State University · USWright State University · US

Funding

Research BaseP30DK072488 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D · 2005 to 2019
$17.3M
Air Pollution and Hypertension: Vascular MechanismsR01ES015146 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI RAJAGOPALAN, SANJAY · 2007 to 2018
$4.5M
Diabetes, Obesity, and Metabolic ComplicationsT32DK098107 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI TAYLOR, SIMEON I. · 2015 to 2025
$2.4M
Diet-Environment Interactions in InflammationR01ES017290 · NIEHS · UNIVERSITY OF MARYLAND BALTIMORE · PI RAJAGOPALAN, SANJAY · 2010 to 2014
$1.8M
Regulation of DPP4 and its non-catalytic function in type 2 diabetesK01DK105108 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHONG, JIXIN · 2015 to 2017
$443k
NIDDK NIH HHS K01 DK105108NIDDK NIH HHS P30 DK072488NIDDK NIH HHS T32 DK098107NIEHS NIH HHS R01 ES015146NIEHS NIH HHS R01 ES017290
6 · The paper itself

Abstract

backgroundInhaled ozone (O3) has been demonstrated as a harmful pollutant and associated with chronic inflammatory diseases such as diabetes and vascular disorders. However, the underlying mechanisms by which O3 mediates harmful effects are poorly understood.

objectivesTo investigate the effect of O3 exposure on glucose intolerance, immune activation and underlying mechanisms in a genetically susceptible mouse model.

methodsDiabetes-prone KK mice were exposed to filtered air (FA), or O3 (0.5 ppm) for 13 consecutive weekdays (4 h/day). Insulin tolerance test (ITT) was performed following the last exposure. Plasma insulin, adiponectin, and leptin were measured by ELISA. Pathologic changes were examined by H&E and Oil-Red-O staining. Inflammatory responses were detected using flow cytometry and real-time PCR.

resultsKK mice exposed to O3 displayed an impaired insulin response. Plasma insulin and leptin levels were reduced in O3-exposed mice. Three-week exposure to O3 induced lung inflammation and increased monocytes/macrophages in both blood and visceral adipose tissue. Inflammatory monocytes/macrophages increased both systemically and locally. CD4 + T cell activation was also enhanced by the exposure of O3 although the relative percentage of CD4 + T cell decreased in blood and adipose tissue. Multiple inflammatory genes including CXCL-11, IFN-γ, TNFα, IL-12, and iNOS were up-regulated in visceral adipose tissue. Furthermore, the expression of oxidative stress-related genes such as Cox4, Cox5a, Scd1, Nrf1, and Nrf2, increased in visceral adipose tissue of O3-exposed mice.

conclusionsRepeated O3 inhalation induces oxidative stress, adipose inflammation and insulin resistance.

Indexed as

Air PollutantsAnimalsGene ExpressionImmunity, InnateInhalation ExposureInsulinInsulin ResistanceLeptinLungMice, Inbred StrainsOxidative StressOzoneAir PollutantsInsulinLeptinOzoneAir pollutioninflammationinsulin resistanceoxidative stressozone exposure

Identifiers

PMID27240593
PMCPMC4911226
OpenAlexW2415564337

What OpenQuestion holds

Textmetadata
LicenceTDM
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.