epigenetic changes in gene ALOX12 associated with persistent wheezing in childhood


Also evaluated the possible effect on the methylation levels of prenatal exposures previously associated with childhood asthma (maternal smoking, use of folate supplements and organochlorine pesticides) andgenetic variants.

This used data from two cohorts of INMA: Menorca (n = 122) and Sabadell (n = 236). Methylation levels in relation to the presence of persistent wheezing were analyzed in a total of 807 genesin the participants of the cohort of Menorca. The results were validatedin the cohort of Menorca and replicated in the cohort of Sabadell by pyrosequencing, the technique gold standard” for quantification of methylation levelsInformation onmaternal smoking and the use of folate supplements during pregnancy was obtainedthrough questionnairesDichlorodiphenyldichloroethylene levels (DDE) were measured in umbilical cord blood or maternal serum.

The results of both studies showed that lower levels of methylation in the gene ALOX12were associated with increased risk of persistent wheezing in childhood. Prenatal exposure to higher levels of DDE was associated with lower levels of methylation in the gene ALOX12 in the cohort of Menorca, although these results were not replicated in the cohort of Sabadell. The results of both studies showed that levels of methylation in the gene variants were associated with ALOX12 underlying genetic.

The most important conclusion of the study is that levels of methylation in the gene ALOX12 epigenetic biomarker may be a risk of developing symptoms of asthma in childhood.


Eva Morales MDMaster in Public Health. Specialist in Preventive Medicine and Public Health and works in the INMA cohort of Sabadell