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Ambient air pollution impairs regulatory T-cell function in asthma.
Kari Nadeau1, Cameron McDonald-Hyman, Elizabeth M Noth
1School of Medicine, Stanford University, Stanford, CA, USA. knadeau@stanford.edu
The Journal of Allergy and Clinical Immunology
|October 6, 2010
Summary
Ambient air pollution (AAP) exposure in children with asthma is linked to epigenetic changes, specifically increased DNA methylation of the Foxp3 gene. This impairs regulatory T-cell function, worsening asthma symptoms and increasing disease severity.
Area of Science:
- Environmental health
- Immunology
- Epigenetics
Background:
- Childhood asthma is a significant health concern, with children being vulnerable to ambient air pollution (AAP).
- Regulatory T (Treg) cells are crucial for immune regulation in asthma, and their function is linked to DNA methylation of the Forkhead box transcription factor 3 (Foxp3) gene.
- AAP exposure can induce epigenetic modifications, prompting an investigation into its impact on Treg-cell function and asthma.
Purpose of the Study:
- To determine if AAP exposure leads to Foxp3 gene hypermethylation.
- To assess if this hypermethylation impairs Treg-cell suppression and exacerbates asthma symptoms.
Main Methods:
- A cross-sectional study involving children with and without asthma from high-pollution (Fresno) and low-pollution (Stanford) areas.
- Analysis of peripheral blood Treg cells for functional and epigenetic markers, including Foxp3 methylation.
- Asthma severity was evaluated using the Global Initiative in Asthma (GINA) score.
Main Results:
- Children in the high-pollution group (Fresno Asthma Group) exhibited impaired Treg-cell suppression and reduced chemotaxis.
- Treg-cell dysfunction in the high-pollution group correlated with lower GINA scores, indicating worse asthma control.
- Significantly higher Foxp3 gene methylation levels were observed in the high-pollution asthma group compared to controls.
Conclusions:
- Increased AAP exposure is associated with hypermethylation of the Foxp3 locus, leading to impaired Treg-cell function.
- This epigenetic alteration in Treg cells may contribute to increased asthma morbidity through immune mechanisms.
- AAP may play a role in exacerbating childhood asthma by mediating epigenetic changes that affect immune regulation.
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