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Published on: April 13, 2017
Passive smoking induces pediatric asthma by affecting the balance of Treg/Th17 cells
Wei Jing1, Wei Wang2, Qingbin Liu2
1Department of Pediatrics, The Affiliated Hospital of Changchun University of Traditional Chinese Medicine, 130021, Changchun, China. jingwei20166@126.com.
Insights
Passive smoking worsens childhood asthma severity by disrupting the balance of T-regulatory (Treg) and T-helper type 17 (Th17) cells. This study quantifies the molecular mechanisms linking environmental tobacco smoke exposure to pediatric asthma.
Area of Science:
- Pediatric Pulmonology
- Immunology
- Environmental Health
Background:
- Childhood asthma is a significant public health concern.
- Environmental tobacco smoke (ETS) exposure is a known risk factor for respiratory diseases.
- The specific molecular pathways linking passive smoking to asthma severity require further elucidation.
Purpose of the Study:
- To investigate the impact of passive smoking on pediatric asthma severity.
- To explore the underlying molecular mechanisms, focusing on T-regulatory (Treg) and T-helper type 17 (Th17) cell balance.
- To correlate environmental tobacco smoke exposure levels with asthma severity markers.
Main Methods:
- 378 children with asthma were categorized by severity (Grades I-IV).
- Environmental tobacco smoke exposure was assessed using urinary cotinine levels.
- Serum immunoglobulin E (IgE), cytokine levels, and peripheral blood mononuclear cell (PBMC) percentages of Treg and Th17 cells were quantified.
- Treg- and Th17-associated transcription factors were measured.
Main Results:
- Higher levels of environmental tobacco smoke exposure and serum IgE correlated with increased asthma severity.
- Passive smoking was associated with decreased levels of FoxP3 and TGF-β (Treg markers).
- Passive smoking increased levels of IL-17A and IL-23 (Th17 markers), significantly reducing the Treg/Th17 cell ratio.
Conclusions:
- Passive smoking is closely linked to increased childhood asthma severity.
- The mechanism involves an imbalance in Treg/Th17 cell populations, favoring a pro-inflammatory state.
- This study highlights the critical role of environmental tobacco smoke in pediatric asthma pathogenesis.
Background:
We aimed to explore the effects of passive smoking on the severity of pediatric asthma and associated molecular mechanisms.
Methods:
A total of 378 children with asthma were assigned into four groups according to asthma severity (from grades I to IV). Univariate and multivariate regression analyses were used to analyze possible factors associated with asthma severity in children. Environmental tobacco smoke (ETS) exposure was measured via cotinine concentration in urine. Serum levels of immunoglobulin E (IgE) and cytokines were measured using allergen diagnostic and ELISA (enzyme-linked immunosorbent assay) kits. The percentage of T-regulatory (Treg) and T-helper type 17 (Th17) cells in peripheral blood mononuclear cells (PMBCs) were measured by flow cytometry. Treg- and Th17-associated transcription factors from PMBCs were measured by using ELISA kits.
Results:
The levels of ETS and serum IgE, and the duration and amounts of passive smoking were closely associated with asthma severity. Passive smoking significantly reduced the levels of FoxP3 (Forkhead/winged helix transcription factor) and tumor growth factor-β, which were associated with Treg cells, and increased the levels of interleukin-17A and interleukin-23, which were associated with Th17 cells. Meanwhile, passive smoking significantly reduced the ratio of Treg/Th17 cells (P < 0.05).
Conclusions:
Passive smoking was closely associated with the severity of childhood asthma by affecting the balance of Treg/Th17 cells.
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