López-Expósito Iván, Song Ying, Järvinen Kirsi M, Srivastava Kamal, Li Xiu-Min
Department of Pediatrics, Mount Sinai School of Medicine, New York, NY 10029-6574, USA.
J Allergy Clin Immunol. 2009 Nov;124(5):1039-46. doi: 10.1016/j.jaci.2009.08.024.
Maternal allergy is believed to be a risk factor for peanut allergy (PNA) in children. However, there is no direct evidence of maternal transmission of PNA susceptibility, and it is unknown whether maternal peanut exposure affects the development of PNA in offspring.
To investigate the influence of maternal PNA on offspring reactions to the first peanut exposure, and whether maternal low-dose peanut exposure during pregnancy and lactation influences these reactions and peanut sensitization in a murine model.
Five-week-old offspring of PNA C3H/HeJ mothers (PNA-Ms) were challenged intragastrically with peanut (first exposure), and reactions were determined. In a subset of the experiment, PNA-Ms were fed a low dose of peanut (PNA-M/PN) or not fed peanut (PNA-M/none) during pregnancy and lactation. Their 5-week-old offspring were challenged intragastrically with peanut, and reactions were determined. In another subset of the experiment, offspring of PNA-M/PN or PNA-M/none were sensitized with peanut intragastrically for 6 weeks, and serum peanut-specific antibodies were determined.
PNA-M offspring exhibited anaphylactic reactions at first exposure to peanut that were associated with peanut-specific IgG(1) levels and prevented by a platelet activation factor antagonist. In a subset experiment, PNA-M/PN offspring showed significantly reduced first-exposure peanut reactions, increased IgG(2a), and reduced mitogen-stimulated splenocyte cytokine production compared with PNA-M/none offspring. In an additional experiment, PNA-M/PN offspring showed reduction of peanut-specific IgE to active peanut sensitization.
We show for the first time maternal transmission of susceptibility to first-exposure peanut reactions and active peanut sensitization. Low-dose peanut exposure during pregnancy and lactation reduced this risk.
母体过敏被认为是儿童花生过敏(PNA)的一个风险因素。然而,尚无PNA易感性母体传播的直接证据,并且母体花生暴露是否会影响后代PNA的发展尚不清楚。
研究母体PNA对后代首次接触花生反应的影响,以及孕期和哺乳期母体低剂量花生暴露是否会影响这些反应以及小鼠模型中的花生致敏作用。
对PNA C3H/HeJ母亲(PNA-Ms)5周龄的后代进行花生灌胃激发(首次接触),并测定反应。在实验的一个子集中,PNA-Ms在孕期和哺乳期喂食低剂量花生(PNA-M/PN)或不喂食花生(PNA-M/无)。对其5周龄的后代进行花生灌胃激发,并测定反应。在实验的另一个子集中,对PNA-M/PN或PNA-M/无的后代进行花生灌胃致敏6周,并测定血清花生特异性抗体。
PNA-M后代在首次接触花生时表现出过敏反应,这与花生特异性IgG(1)水平相关,并可被血小板活化因子拮抗剂阻断。在一个子集实验中,与PNA-M/无的后代相比,PNA-M/PN后代首次接触花生的反应显著降低,IgG(2a)增加,丝裂原刺激的脾细胞细胞因子产生减少。在另一项实验中,PNA-M/PN后代对活性花生致敏的花生特异性IgE减少。
我们首次证明了母体将首次接触花生反应和活性花生致敏的易感性进行了传递。孕期和哺乳期低剂量花生暴露降低了这种风险。