The effect of secondhand smoking exposure and IL-17 gene polymorphism on childhood asthma

Asthma affects 300 million people worldwide. Multiple genes, environmental factors, and their interactions have been associated with asthma. Smoking has been shown to play an essential role in pathogenesis by triggering an IL-17-mediated inflammatory response. This study investigates the effect of IL-17 polymorphism and its interaction with smoking on pediatric asthma. The purpose was to gain a better understanding of the impact of smoking on the development of asthma and to determine whether genetic predisposition contributes to the variability of the inflammatory response induced by smoking. The study included 100 asthma patients and 100 healthy children. The genetic study was conducted on all children, demonstrating IL-17F (rs763780) and IL-17A (rs8193036, rs2275913) polymorphisms. Serum cotinine levels were measured using the ELISA method to maintain secondhand smoking exposure (SHSe). In our study, the cut-off point for SHSe was identified as 11.06, the sample median. The study participants were categorized into four groups based on the threshold: asthma with SHSe, asthma without SHSe, control with SHSe, and control without SHSe. The median value of cotinine was 11,06 ng/mL. The SNP genotype distribution and allele frequency of rs763780, rs8193036, and rs2275913 were compared between the four groups, and no significant difference was found. This study is the first to demonstrate the relationship between IL-17 polymorphisms and smoking interaction in childhood asthma. Neither IL-17 polymorphisms nor their interaction with smoking was found to be associated with pediatric asthma. It has been observed that SHSe in children is still a significant public health issue in our nation.