Passive smoking induces pediatric asthma by affecting the balance of Treg/Th17 cells.

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.