Prenatal allergen exposures prevent allergen‐induced sensitization and airway inflammation in young mice
Prenatal allergen exposures prevent allergen‐induced sensitization and airway inflammation in young mice
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产前过敏原暴露可预防幼鼠过敏原诱导的过敏和气道炎症
DOI：
10.1111/j.1398-9995.2011.02775.x
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发表时间：
2012
期刊：
影响因子：
12.4
通讯作者：
E. Hamelmann
中科院分区：
文献类型：
--
作者：
Gerhold;A. Avagyan;E. Reichert;C. Seib;D.V. Van;E.O. Luger;A. Hutloff;E. Hamelmann
免疫调节，如耐受诱导似乎是一个即将到来的概念，以防止特应性疾病的发展。妊娠期可能是预防后代过敏性致敏的关键时期。我们研究了在怀孕期间母体过敏原暴露对过敏原诱导的致敏和气道炎症的后代在murine model.MethodsBALB/c小鼠暴露于雾化卵清蛋白（OVA），每周三次，从怀孕第7天，直到交付（0天）的影响。在第48、49和50天进行气道过敏原激发之前，在出生后第21和35天之间通过6次腹腔内注射OVA对后代进行全身致敏。在第52天进行分析。为了检查母体OVA暴露的长期影响，在第115天和第129天之间对一些后代进行致敏;在第147天进行分析。结果与母体安慰剂暴露相比，母体OVA暴露抑制了OVA致敏后代在第52天和第147天的OVA特异性IgE血清水平，并抑制了过敏原诱导的气道炎症的发展。这种保护作用与从主要Th 2免疫应答向主要产生细胞因子IFN-γ和IL-10的转变有关。此外，母体OVA暴露与OVA致敏后代中CD 25 + Foxp 3+调节性T细胞（TCRs）的发育相关。在过敏原致敏之前，Tregsor中和IL-10的耗竭在OVA致敏的后代中重新建立了OVA诱导的致敏和嗜酸性粒细胞气道炎症。ConclusionsIn our model，maternal allergen exposure during pregnancy prevents later allergen介导的致敏和气道炎症by allergen specific tolerance induction in the children.
BackgroundImmune‐modulation such as tolerance induction appears to be an upcoming concept to prevent development of atopic diseases. Pregnancy might present a critical period for preventing allergic sensitization of the progeny. We investigated the effect of maternal allergen exposures during pregnancy on allergen‐induced sensitization and airway inflammation in the offspring in a murine model.MethodsBALB/c mice were exposed to aerosolized ovalbumin (OVA) three times per week from day 7 of pregnancy until delivery (day 0). Offspring were systemically sensitized by six intraperitoneal injections with OVA between postnatal days 21 and 35, prior to airway allergen challenges on days 48, 49, and 50. Analyses were performed on day 52. To examine long‐lasting effects of maternal OVA exposures some offspring were sensitized between days 115 and 129; analyses took place on day 147.ResultsCompared to maternal placebo exposures, maternal OVA exposures suppressed OVA‐specific IgE serum levels and inhibited development of allergen‐induced airway inflammation in the OVA‐sensitized offspring on both days 52 and 147. This protective effect was associated with a shift from a predominant Th2 immune response toward a predominant production of the cytokines IFN‐γ and IL‐10. Further, maternal OVA exposures were associated with development of CD25+Foxp3+regulatory T cells (Tregs) in the OVA‐sensitized offspring. Depletion of Tregsor neutralization of IL‐10 prior to allergen sensitization re‐established OVA‐induced sensitization and eosinophilic airway inflammation in the OVA‐sensitized offspring.ConclusionsIn our model, maternal allergen exposures during pregnancy prevented later allergen‐mediated sensitization and airway inflammation by allergen‐specific tolerance induction in the offspring.
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影响因子：
14.2
作者：
Polte, Tobias;Hennig, Christian;Hansen, Gesine
通讯作者：
Hansen, Gesine
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影响因子：
3.3
作者：
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V. Verhasselt
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影响因子：
56.9
作者：
X. Hiteshbhai
通讯作者：
X. Hiteshbhai
影响因子：
6.4
作者：
Fusaro, Ana E.;Brito, Cyro A.;Sato, Maria N.
通讯作者：
Sato, Maria N.
影响因子：
4.4
作者：
Nwaru, Bright I.;Ahonen, Suvi;Virtanen, Suvi M.
通讯作者：
Virtanen, Suvi M.