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Background  Epigenetic modifications, including DNA methylation, act as one potential mechanism underlying the detrimental effects associated with prenatal tobacco smoke (PTS) exposure. Methylation in a gene called  AXL  was previously reported to differ in response to PTS.    Methods  We investigated the association between PTS and epigenetic changes in  AXL  and how this was related to childhood asthma phenotypes. We tested the association between PTS and DNA methylation at multiple CpG loci of  AXL  at birth using Pyrosequencing in two separate study populations, the Children’s Health Study (CHS, n = 799) and the Newborn Epigenetic Study (NEST, n = 592). Plasma cotinine concentration was used to validate findings with self-reported smoking status. The inter-relationships among  AXL  mRNA and miR-199a1 expression, PTS, and  AXL  methylation were examined. Lastly, we evaluated the joint effects of  AXL  methylation and PTS on the risk of asthma and related symptoms at age 10 years old.    Results  PTS was associated with higher methylation level in the  AXL  gene body in both CHS and NEST subjects. In the pooled analysis, exposed subjects had a 0.51% higher methylation level in this region compared to unexposed subjects (95% CI 0.29, 0.74;  p  < 0.0001). PTS was also associated with 21.2% lower expression of miR-199a1 (95% CI − 37.9, − 0.1;  p  = 0.05), a microRNA known to regulate  AXL  expression. Furthermore, the combination of higher  AXL  methylation and PTS exposure at birth increased the risk of recent episodes of bronchitic symptoms in childhood.    Conclusions  PTS was associated with methylation level of  AXL  and the combination altered the risk of childhood bronchitic symptoms.    Electronic supplementary material  The online version of this article (10.1186/s13148-018-0532-x) contains supplementary material, which is available to authorized users.

Self-reported prenatal tobacco smoke exposure, AXL gene-body methylation, and childhood asthma phenotypes