scholarly journals Exposure to Traffic-Related Air Pollution and Changes in Exhaled Nitric Oxide and DNA Methylation in Arginase and Nitric Oxide Synthase in Children with Asthma

2020 ◽  
Author(s):  
Nan Ji ◽  
Mingzhu Fang ◽  
Ana Baptista ◽  
Clarimel Cepeda ◽  
Molly Greenberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Methylation ◽  
Air Pollution ◽  
Nitric Oxide Synthase ◽  
Airway Inflammation ◽  
Personal Exposure ◽  
Epigenetic Changes ◽  
Promoter Regions ◽  
Children With Asthma ◽  
Oxide Synthase

Abstract Background: Traffic-related air pollution (TRAP) has been associated with increased risk of airway inflammation in children with asthma. While epigenetic changes could potentially modulate TRAP-induced inflammatory responses, few studies have assessed the temporal pattern of exposure to TRAP, epigenetic changes and inflammation in children with asthma. Our goal was to test the time-lag patterns of personal exposure to TRAP, airway inflammation (measured as fractional exhaled nitric oxide, FeNO), and DNA methylation in the promoter regions of genes involved in nitric oxide synthesis among children with asthma.Methods: We measured personal exposure to black carbon (BC) and FeNO for up to 30 days in a panel of children with asthma. We collected 90 buccal cell samples for DNA methylation analysis from 18 children (5 per child). Methylation in promoter regions of nitric oxide synthase (NOS1, NOS2A, NOS3) and arginase (ARG1, ARG2) was assessed by bisulfite pyrosequencing. Linear-mixed effect models were used to test the associations of BC at different lag periods, percent DNA methylation at each site and FeNO level.Results: Exposure to BC was positively associated with FeNO, and negatively associated with DNA methylation in NOS3. We found strongest association between FeNO and BC at lag 0–6 hours while strongest associations between methylation at positions 1 and 2 in NOS3 and BC were at lag 13-24 hours and lag 0-24 hours, respectively. The strengths of associations were attenuated at longer lag periods. No significant associations between exposure to TRAP and methylation levels in other NOS and ARG isoforms were observed.Conclusions: Exposure to TRAP was associated with higher levels of FeNO and lower levels of DNA methylation in the promoter regions of the NOS3 gene, indicating that DNA methylation of the NOS3 gene could be an important epigenetic mechanism in physiological responses to TRAP in children with asthma.

scholarly journals Exposure to traffic-related air pollution and changes in exhaled nitric oxide and DNA methylation in arginase and nitric oxide synthase in children with asthma

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
N. Ji ◽  
M. Fang ◽  
A. Baptista ◽  
C. Cepeda ◽  
M. Greenberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Methylation ◽  
Air Pollution ◽  
Nitric Oxide Synthase ◽  
Airway Inflammation ◽  
Personal Exposure ◽  
Epigenetic Changes ◽  
Promoter Regions ◽  
Children With Asthma ◽  
Oxide Synthase

Abstract Background Traffic-related air pollution (TRAP) has been associated with increased risk of airway inflammation in children with asthma. While epigenetic changes could potentially modulate TRAP-induced inflammatory responses, few studies have assessed the temporal pattern of exposure to TRAP, epigenetic changes and inflammation in children with asthma. Our goal was to test the time-lag patterns of personal exposure to TRAP, airway inflammation (measured as fractional exhaled nitric oxide, FeNO), and DNA methylation in the promoter regions of genes involved in nitric oxide synthesis among children with asthma. Methods We measured personal exposure to black carbon (BC) and FeNO for up to 30 days in a panel of children with asthma. We collected 90 buccal cell samples for DNA methylation analysis from 18 children (5 per child). Methylation in promoter regions of nitric oxide synthase (NOS1, NOS2A, NOS3) and arginase (ARG1, ARG2) was assessed by bisulfite pyrosequencing. Linear-mixed effect models were used to test the associations of BC at different lag periods, percent DNA methylation at each site and FeNO level. Results Exposure to BC was positively associated with FeNO, and negatively associated with DNA methylation in NOS3. We found strongest association between FeNO and BC at lag 0–6 h while strongest associations between methylation at positions 1 and 2 in NOS3 and BC were at lag 13–24 h and lag 0–24 h, respectively. The strengths of associations were attenuated at longer lag periods. No significant associations between exposure to TRAP and methylation levels in other NOS and ARG isoforms were observed. Conclusions Exposure to TRAP was associated with higher levels of FeNO and lower levels of DNA methylation in the promoter regions of the NOS3 gene, indicating that DNA methylation of the NOS3 gene could be an important epigenetic mechanism in physiological responses to TRAP in children with asthma.

scholarly journals Exposure to Traffic-Related Air Pollution and Changes in Exhaled Nitric Oxide and DNA Methylation in Arginase and Nitric Oxide Synthase in Children with Asthma

2020 ◽  
Author(s):  
Nan Ji ◽  
Mingzhu Fang ◽  
Ana Baptista ◽  
Clarimel Cepeda ◽  
Molly Greenberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Methylation ◽  
Air Pollution ◽  
Nitric Oxide Synthase ◽  
Personal Exposure ◽  
Epigenetic Changes ◽  
Promoter Regions ◽  
Nos3 Gene ◽  
Children With Asthma ◽  
Oxide Synthase

Abstract Background Traffic-related air pollution (TRAP) has been associated with increased risk of airway inflammation in children with asthma. While epigenetic changes could potentially modulate TRAP-induced inflammatory responses, few studies have assessed the temporal pattern of exposure to TRAP, epigenetic changes and inflammation in children with asthma. Our goal was to test the time-lag patterns of personal exposure to TRAP, airway inflammation (measured as fractional exhaled nitric oxide, FeNO), and DNA methylation in the promoter regions of genes involved in nitric oxide synthesis among children with asthma. Methods We measured personal exposure to black carbon (BC) and FeNO for up to 30 days in a panel of children with asthma. We collected 90 buccal cell samples for DNA methylation analysis from 18 children (5 per child). Methylation in promoter regions of nitric oxide synthase (NOS1, NOS2A, NOS3) and arginase (ARG1, ARG2) was assessed by bisulfite pyrosequencing. Linear-mixed effect models were used to test the associations of BC at different lag periods, percent DNA methylation at each site and FeNO level. Results Exposure to BC was positively associated with FeNO, and negatively associated with DNA methylation in NOS3. We found strongest association between FeNO and BC at lag 0–6 hours while strongest associations between methylation at positions 1 and 2 in NOS3 and BC were at lag 13–24 hours and lag 0–24 hours, respectively. The strengths of associations were attenuated at longer lag periods. No significant associations between exposure to TRAP and methylation levels in other NOS and ARG isoforms were observed. Conclusions Exposure to TRAP was associated with higher levels of FeNO and lower levels of DNA methylation in the promoter regions of the NOS3 gene, indicating that DNA methylation of the NOS3 gene could be an important epigenetic mechanism in physiological responses to TRAP in children with asthma.

Air Pollution Is Associated With DNA Methylation In Nitric Oxide Synthase

2011 ◽  
Author(s):  
Carrie Breton ◽  
Hyang-Min Byun ◽  
Xinhui Wang ◽  
Muhammad T. Salam ◽  
Kimberly D. Siegmund ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dna Methylation ◽  
Air Pollution ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase

Plasma arginine metabolites reflect airway dysfunction in a murine model of allergic airway inflammation

2015 ◽  
Vol 118 (10) ◽  
pp. 1229-1233 ◽  
Author(s):  
Jeremy A. Scott ◽  
Michelle L. North ◽  
Mahrouk Rafii ◽  
Hailu Huang ◽  
Paul Pencharz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Airway Inflammation ◽  
Plasma Concentrations ◽  
Allergic Airway Inflammation ◽  
Airway Responsiveness ◽  
Arginase Activity ◽  
Therapeutic Interventions ◽  
Oxide Synthase

l-Arginine metabolism is important in the maintenance of airway tone. Shift of metabolism from the nitric oxide synthase to arginase pathways contributes to the increased airway responsiveness in asthma. We tested the hypothesis that systemic levels of l-arginine metabolites are biomarkers reflective of airway dysfunction. We used a mouse model of acute allergic airway inflammation to OVA that manifests with significant airway hyperresponsiveness to methacholine. To determine tissue arginase activity in vivo, the isotopic enrichment of an infused l-arginine stable isotope and its product amino acid l-ornithine were measured in lung and airway homogenates using liquid chromatography-tandem mass spectrometry. Tissue and plasma concentrations of other l-arginine metabolites, including l-citrulline and symmetric and asymmetric dimethylarginine, were measured and correlated with lung arginase activity and methacholine responsiveness of the airways. The effectiveness of intratracheal instillation of an arginase inhibitor (boronoethylcysteine) on pulmonary arginase activity and circulating concentrations of l-arginine metabolites was also studied. We demonstrate that 1) plasma indexes of l-arginine bioavailability and impairment of nitric oxide synthase function correlate with airway responsiveness to methacholine; 2) plasma levels of l-ornithine predict in vivo pulmonary arginase activity and airway function; and 3) acute arginase inhibition reduces in vivo pulmonary arginase activity to control levels and normalizes plasma l-ornithine, but not l-arginine, bioavailability in this model. We conclude that plasma l-ornithine may be useful as a systemic biomarker to predict responses to therapeutic interventions targeting airway arginase in asthma.

scholarly journals CTLA4-Ig inhibits allergic airway inflammation by a novel CD28-independent, nitric oxide synthase-dependent mechanism

2010 ◽  
Vol 40 (7) ◽  
pp. 1985-1994 ◽  
Author(s):  
Christine M. Deppong ◽  
Amit Parulekar ◽  
Jonathan S. Boomer ◽  
Traci L. Bricker ◽  
Jonathan M. Green
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Oxide Synthase ◽  
Dependent Mechanism
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