ArticleThe European respiratory journal2010
Identification of novel susceptibility genes in ozone-induced inflammation in mice.
Article in The European respiratory journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Transcriptomics Underlying Pulmonary Ozone Pathogenesis Regulated by Inflammatory Mediators in Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Transcriptional Effects of Ozone and Impact on Airway Inflammation.Frontiers in immunology · 2019Review
- Inactivation of TNF/LT locus alters mouse metabolic response to concentrated ambient PMToxicology · 2017Article
- Inflammasome, IL-1 and inflammation in ozone-induced lung injury.American journal of clinical and experimental immunology · 2016Review
- Novel Roles for Notch3 and Notch4 Receptors in Gene Expression and Susceptibility to Ozone-Induced Lung Inflammation in Mice.Environmental health perspectives · 2015Article
- γδ T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice.PloS one · 2015Article
- γδ T cells are required for pulmonary IL-17A expression after ozone exposure in mice: role of TNFα.PloS one · 2014Article
- Individuals with increased inflammatory response to ozone demonstrate muted signaling of immune cell trafficking pathways.Respiratory research · 2012Article
- Identification of candidate genes downstream of TLR4 signaling after ozone exposure in mice: a role for heat-shock protein 70.Environmental health perspectives · 2011Article
- Ambient ozone and pulmonary innate immunity.Immunologic research · 2011Review
- Protective role of interleukin-10 in ozone-induced pulmonary inflammation.Environmental health perspectives · 2010Article
- Toxicogenetics: population-based testing of drug and chemical safety in mouse models.Pharmacogenomics · 2010Review
- Update in environmental and occupational medicine 2009.American journal of respiratory and critical care medicine · 2010Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Ozone (O(3)) remains a prevalent air pollutant and public health concern. Inf2 is a significant quantitative trait locus on murine chromosome 17 that contributes to susceptibility to O(3)-induced infiltration of polymorphonuclear leukocytes (PMNs) into the lung, but the mechanisms of susceptibility remain unclear. The study objectives were to confirm and restrict Inf2, and to identify and test novel candidate susceptibility gene(s). Congenic strains of mice that contained overlapping regions of Inf2 and their controls, and mice deficient in either major histocompatibility complex (MHC) class II genes or the Tnf cluster, were exposed to air or O(3). Lung inflammation and gene expression were assessed. Inf2 was restricted from 16.42 Mbp to 0.96 Mbp, and bioinformatic analysis identified MHC class II, the Tnf cluster and other genes in this region that contain potentially informative single nucleotide polymorphisms between the susceptible and resistant mice. Furthermore, O(3)-induced inflammation was significantly reduced in mice deficient in MHC class II genes or the Tnf cluster genes, compared with wild-type controls. Gene expression differences were also observed in MHC class II and Tnf cluster genes. This integrative genetic analysis of Inf2 led to identification of novel O(3) susceptibility genes that may provide important, new therapeutic targets in susceptible individuals.
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Registered trials
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.