Interaction between secondhand smoke exposure and IL-17 gene polymorphism in pediatric asthma

Asthma is a multifactorial disease affecting approximately 300 million people worldwide. Multiple genes, environmental risk factors, and their interactions have been associated with asthma. Smoking triggers an IL-17-mediated inflammatory response. The IL-17-related inflammatory response may differ between individuals, and this difference is associated with IL-17 polymorphisms.

Our aim was to investigate the effect of IL-17 polymorphism and its interaction with secondhand smoke on pediatric asthma.

The study comprised 100 pediatric asthma patients and 100 healthy children. Cotinine levels were analyzed to show SHS exposure (SHSe). A genetic study was conducted to reveal IL-17F(rs763780) and IL-17A (rs8193036, rs2275913) polymorphisms. The study participants were categorized into four groups based on the cotinine results: asthma with SHSe, asthma without SHSe, control with SHSe, and control without SHSe.

The median cotinine concentration was 11.06 ng/ml. Children with asthma had lower cotinine levels than healthy children (p < 0.001). Genotype distributions and allele frequencies of rs763780, rs8193036, and rs2275913 were compared among the four groups, and no significant differences were found.

This study is the first to demonstrate the relationship between IL-17 polymorphisms and SHS interaction in childhood asthma. Neither the presence of IL-17 polymorphisms nor the interaction of these polymorphisms with SHS was found to be associated. The lower cotinine levels in asthmatic children suggest that parents are more susceptible to SHSe. Cotinine levels in our cohort were significantly greater than those found in developed countries. This demonstrates that exposure to SHS is still a serious environmental issue in our country.