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Background    AXL  is one of the TAM ( TYRO3 ,  AXL  and  MERTK ) receptor tyrosine kinases and may affect numerous immune-related health conditions. However, the role for  AXL  in asthma, including its epigenetic regulation, has not been extensively studied.    Methods  We investigated the association between  AXL  DNA methylation at birth and risk of childhood asthma symptoms at age 6 years. DNA methylation of multiple CpG loci across the regulatory regions of  AXL  was measured in newborn bloodspots using the Illumina HumanMethylation450 array on a subset of 246 children from the Children’s Health Study (CHS). Logistic regression models were fitted to assess the association between asthma symptoms and DNA methylation. Findings were evaluated for replication in a separate population of 1038 CHS subjects using Pyrosequencing on newborn bloodspot samples.  AXL  genotypes were extracted from genome-wide data.    Results  Higher average methylation of CpGs in the  AXL  gene at birth was associated with higher risk of parent-reported wheezing, and the association was stronger in girls than in boys. This relationship reflected the methylation status of the gene-body region near the 5′ end, for which a 1% higher methylation level was significantly associated with a 72% increased risk of ever having wheezed by 6 years. The association of one CpG locus, cg00360107 was replicated using Pyrosequencing. Increased  AXL  methylation was also associated with lower mRNA expression level of this gene in lung tissue from the Cancer Genome Atlas (TCGA) dataset. Furthermore,  AXL  DNA methylation was strongly linked to underlying genetic polymorphisms.    Conclusions    AXL  DNA methylation at birth was associated with higher risk for asthma-related symptoms in early childhood.    Electronic supplementary material  The online version of this article (10.1186/s13148-017-0421-8) contains supplementary material, which is available to authorized users.

Epigenetic regulation of AXL and risk of childhood asthma symptoms