Miller Rachel L, Zhang Hanjie, Jezioro Jacqueline, De Planell Saguer Mariangels, Lovinsky-Desir Stephanie, Liu Xinhua, Perzanowski Matthew, Divjan Adnan, Phipatanakul Wanda, Matsui Elizabeth C
Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Columbia University Medical Center, PH8E-101B, 630 W. 168th St., New York City, NY 10032, USA; Division of Allergy, Immunology, and Rheumatology, Department of Pediatrics, Columbia University Medical Center, PH8E-101B, 630 W. 168th St., New York City, NY 10032, USA; Department of Environmental Health Sciences, Columbia University, 722 W 168th St, 11th Floor, New York City, NY, 10032, USA.
Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, Columbia University Medical Center, PH8E-101B, 630 W. 168th St., New York City, NY 10032, USA.
Environ Res. 2017 Jul;156:619-624. doi: 10.1016/j.envres.2017.04.025. Epub 2017 Apr 26.
Chronic exposure to mouse allergen may contribute greatly to the inner-city asthma burden. We hypothesized that reducing mouse allergen exposure may modulate the immunopathology underlying symptomatic pediatric allergic asthma, and that this occurs through epigenetic regulation. To test this hypothesis, we studied a cohort of mouse sensitized, persistent asthmatic inner-city children undergoing mouse allergen-targeted integrated pest management (IPM) vs education in a randomized controlled intervention trial. We found that decreasing mouse allergen exposure, but not cockroach, was associated with reduced FOXP3 buccal DNA promoter methylation, but this was unrelated to mouse specific IgE production. This finding suggests that the environmental epigenetic regulation of an immunomodulatory gene may occur following changing allergen exposures in some highly exposed cohorts. Given the clinical and public health importance of inner-city pediatric asthma and the potential impact of environmental interventions, further studies will be needed to corroborate changes in epigenetic regulation following changing exposures over time, and determine their impact on asthma morbidity in susceptible children.
长期接触小鼠过敏原可能极大地加重城市内哮喘负担。我们推测，减少小鼠过敏原接触可能调节有症状的儿童过敏性哮喘潜在的免疫病理学，并且这是通过表观遗传调控发生的。为了验证这一假设，我们在一项随机对照干预试验中，研究了一组对小鼠致敏的、患有持续性哮喘的城市内儿童，他们接受了针对小鼠过敏原的综合虫害管理（IPM）与教育。我们发现，减少小鼠过敏原接触而非蟑螂过敏原接触，与FOXP3口腔DNA启动子甲基化减少有关，但这与小鼠特异性IgE产生无关。这一发现表明，在一些高暴露队列中，过敏原接触改变后可能会发生免疫调节基因的环境表观遗传调控。鉴于城市内儿童哮喘的临床和公共卫生重要性以及环境干预的潜在影响，需要进一步研究来证实随着时间推移接触改变后表观遗传调控的变化，并确定它们对易感儿童哮喘发病率的影响。
