|Title||Methylation profiles of IL33 and CCL26 in bronchial epithelial cells are associated with asthma.|
|Publication Type||Journal Article|
|Year of Publication||2018|
|Auteurs||Larouche, M, Gagné-Ouellet, V, Boucher-Lafleur, A-M, Larose, M-C, Plante, S, Madore, A-M, Laviolette, M, Flamand, N, Chakir, J, Laprise, C|
|Date Published||2018 Dec|
|Keywords||Adult, Alleles, Asthma, Chemokine CCL26, DNA Methylation, Eosinophils, Epigenomics, Epithelial Cells, Female, Gene Expression Regulation, Haplotypes, Humans, Interleukin-1 Receptor-Like 1 Protein, Interleukin-33, Lung, Male, Middle Aged, Mutation, Promoter Regions, Genetic, Young Adult|
AIM: This study aimed to characterize DNA methylation (DNA-me) in promoter region of IL33, IL1RL1 and CCL26 in asthma and their impacts on transcriptional activity in bronchial epithelial cells (BECs).PATIENTS & METHODS: We performed bis-pyrosequencing, quantitative real-time PCR and sequencing in BECs from ten asthmatic and ten control individuals.RESULTS: We detected lower DNA-me levels of IL33 and CCL26 in asthmatic than control BECs. No correlation was found between methylation and expression levels. Interestingly, carriers of a mutative allele in a haplotype within the promoter of IL33 had a lower IL33 DNA-me level and CCL26 gene expression correlated with eosinophil count.CONCLUSION: These findings highlight the importance of investigating both epigenetic and genetic mechanisms in understanding the epithelial immune response in asthma.
|Grant List||/ / CIHR / Canada|