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Paternal Tobacco Smoke Correlated to Offspring Asthma and Prenatal Epigenetic Programming
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A4162 - Paternal Tobacco Smoke Correlated to Offspring Asthma and Prenatal Epigenetic Programming
Author Block: K. D. Yang1, C. Wu2, C. Chen3; 1Mackay Children's Hospital, Mackay Memorial Hospital, Taipei, Taiwan, 2Pediatrics, Po-Zen Hospital, Kaohsiung, Taiwan, 3Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan.
Introduction: Effects of paternal tobacco smoke (PTS) on the offspring’s asthma and its epigenetic programming are not well-known. This study investigated whether prenatal exposure of PTS was associated with the offspring’s asthma correlated to epigenetic CG methylation of potential tobacco-related immune genes. Methods: A birth cohort follow up of newborns with and without PTS to 6 years of age. Prenatal exposure of PTS, cord blood DNA methylation, infant infection, childhood DNA methylation and childhood allergic diseases were studied and correlated. We completed the follow up of 1348 infants at 18 months of age and 756 children at 6 years of age. Participants were 1629 newborns and their parents. The exposure rates of PTS and maternal tobacco smoke (MTS) exposure were respectively 23.0% and 0.2%. This cohort is therefore suitable for studying effects of prenatal PTS exposure on the offspring’s asthma. Results: Infants with exposure of PTS had a significantly higher rate of upper respiratory tract infections (URIs) at age of 18 months (p=0.007), and a significantly higher risk of asthma by age of 6 than those without (p=0.026). The LMO2_P794 and IL10_P325 CG methylation levels detected were individually associated with prenatal PTS exposure (p=0.005 and p=0.033, respectively), and the LMO2_P794 methylation content was associated with physician-diagnosed asthma (p=0.019). Using receiver operating characteristic curve to cut off risk methylation levels, the combination of higher CG methylation levels of LMO2_E148, IL10_P325 and GSTM1_P266 corresponded to the highest risk of asthma by 43.48%, compared to other combinations (16.67%-23.08%) in the 3-way multi-factor dimensionality reduction (MDR) analysis. The LMO2_P794 and GSTM1_P266 CG methylation levels at age 0 were significantly correlated to those at age of 6. Conclusions: Prenatal exposure of PTS can program epigenetic CG methylation of LMO2, GSTM1 and IL-10, which is retained into childhood and associated with development of asthma. Clarifying the prenatal epigenetic program of PTS for childhood asthma may provide a novel regimen to modulate the epigenetic program and its related mRNA or protein expression of the immune regulation genes for the early prediction and prevention of childhood asthma.
Author Block: K. D. Yang1, C. Wu2, C. Chen3; 1Mackay Children's Hospital, Mackay Memorial Hospital, Taipei, Taiwan, 2Pediatrics, Po-Zen Hospital, Kaohsiung, Taiwan, 3Obstetrics and Gynecology, Mackay Memorial Hospital, Taipei, Taiwan.
Introduction: Effects of paternal tobacco smoke (PTS) on the offspring’s asthma and its epigenetic programming are not well-known. This study investigated whether prenatal exposure of PTS was associated with the offspring’s asthma correlated to epigenetic CG methylation of potential tobacco-related immune genes. Methods: A birth cohort follow up of newborns with and without PTS to 6 years of age. Prenatal exposure of PTS, cord blood DNA methylation, infant infection, childhood DNA methylation and childhood allergic diseases were studied and correlated. We completed the follow up of 1348 infants at 18 months of age and 756 children at 6 years of age. Participants were 1629 newborns and their parents. The exposure rates of PTS and maternal tobacco smoke (MTS) exposure were respectively 23.0% and 0.2%. This cohort is therefore suitable for studying effects of prenatal PTS exposure on the offspring’s asthma. Results: Infants with exposure of PTS had a significantly higher rate of upper respiratory tract infections (URIs) at age of 18 months (p=0.007), and a significantly higher risk of asthma by age of 6 than those without (p=0.026). The LMO2_P794 and IL10_P325 CG methylation levels detected were individually associated with prenatal PTS exposure (p=0.005 and p=0.033, respectively), and the LMO2_P794 methylation content was associated with physician-diagnosed asthma (p=0.019). Using receiver operating characteristic curve to cut off risk methylation levels, the combination of higher CG methylation levels of LMO2_E148, IL10_P325 and GSTM1_P266 corresponded to the highest risk of asthma by 43.48%, compared to other combinations (16.67%-23.08%) in the 3-way multi-factor dimensionality reduction (MDR) analysis. The LMO2_P794 and GSTM1_P266 CG methylation levels at age 0 were significantly correlated to those at age of 6. Conclusions: Prenatal exposure of PTS can program epigenetic CG methylation of LMO2, GSTM1 and IL-10, which is retained into childhood and associated with development of asthma. Clarifying the prenatal epigenetic program of PTS for childhood asthma may provide a novel regimen to modulate the epigenetic program and its related mRNA or protein expression of the immune regulation genes for the early prediction and prevention of childhood asthma.
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