Fedulov Alexey V, Leme Adriana S, Kobzik Lester
Department of Environmental Health, Harvard School of Public Health, Boston, MA 02115, USA.
Am J Reprod Immunol. 2007 Aug;58(2):120-8. doi: 10.1111/j.1600-0897.2007.00496.x.
Asthma has its origins in early-life. Maternal, not paternal asthma is an important risk factor, but the mechanisms and the duration of the maternal effect are unknown.
Offspring of asthmatic and normal mice were sensitized with ovalbumin (OVA) at 1, 3, 6 and 10 weeks of age, challenged with aerosolized OVA 2 weeks later and tested for airway hyperresponsiveness (AHR) and allergic airway inflammation (AI).
Offspring of asthmatic, but not normal, mothers showed AHR and AI after OVA sensitization at week 1. Similarly increased susceptibility to OVA was observed when sensitized at 3 or 6 weeks, although the magnitude diminished. Offspring sensitized at 10 and challenged at 12 weeks showed some AI but no AHR.
In offspring from asthmatic mothers increased allergic susceptibility persisted through the young adulthood, albeit with gradual decline, which suggests a long-lived but reversible skewing of the developing immune system.
哮喘起源于生命早期。母亲而非父亲患哮喘是一个重要的风险因素,但母体影响的机制和持续时间尚不清楚。
哮喘小鼠和正常小鼠的后代在1、3、6和10周龄时用卵清蛋白(OVA)致敏,2周后用雾化OVA激发,并检测气道高反应性(AHR)和过敏性气道炎症(AI)。
哮喘母亲的后代在第1周用OVA致敏后出现AHR和AI,而正常母亲的后代未出现。同样,在3周或6周致敏时,对OVA的易感性也增加,尽管程度有所减轻。在10周致敏并在12周激发的后代表现出一些AI,但没有AHR。
哮喘母亲的后代在成年早期仍存在过敏易感性增加的情况,尽管有逐渐下降的趋势,这表明发育中的免疫系统存在长期但可逆的偏差。