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首页> 外文期刊>Life sciences >Single early prenatal lipopolysaccharide exposure prevents subsequent airway inflammation response in an experimental model of asthma.
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Single early prenatal lipopolysaccharide exposure prevents subsequent airway inflammation response in an experimental model of asthma.

机译：在哮喘的实验模型中，单次早期产前脂多糖暴露可防止随后的气道炎症反应。

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AIMS: There has been emerging interest in the prenatal determinants of respiratory disease. In utero factors have been reported to play a role in airway development, inflammation, and remodeling. Specifically, prenatal exposure to endotoxins might regulate tolerance to allergens later in life. The present study investigated whether prenatal lipopolysaccharide (LPS) administration alters subsequent offspring allergen-induced inflammatory response in adult rats. MAIN METHODS: Pregnant Wistar rats were treated with LPS (100 mug/kg, i.p.) on gestation day 9.5 and their ovariectomized female offspring were sensitized and challenged with OVA later in adulthood. The bronchoalveolar lavage (BAL) fluid, peripheral blood, bone marrow leukocytes and passive cutaneous anaphylaxis were evaluated in these 75-day-old pups. KEY FINDINGS: OVA sensitized pups of NaCl treated rats showed an increase of leucocytes in BAL after OVA challenge. This increase was attenuated, when mothers were exposed to a single LPS injection early in pregnancy. Thus, LPS prenatal treatment resulted in (1) lower increased total and differential (macrophages, neutrophils, eosinophils and lymphocytes) BAL cellularity count; (2) increased number of total, mononuclear and polymorphonuclear cells in the peripheral blood; and (3) no differences in bone marrow cellularity or passive cutaneous anaphylaxis. SIGNIFICANCE: In conclusion, female pups treated prenatally with LPS presented an attenuated response to experimentally-induced asthma. We observed reduced immune cell migration from peripheral blood to the lungs, with no effect on the production of bone marrow cells or antibodies. It was suggested that inflammatory events such as exposure to LPS in early fetal life can attenuate allergic inflammation in the lung, which is a common symptom in asthma.
机译：目的：人们对呼吸道疾病的产前决定因素产生了兴趣。据报道子宫内因素在气道发育，炎症和重塑中起作用。特别是，产前暴露于内毒素可能会在以后的生活中调节对过敏原的耐受性。本研究调查了产前脂多糖（LPS）施用是否会改变成年大鼠随后的后代变应原诱导的炎症反应。主要方法：妊娠Wistar大鼠在妊娠第9.5天接受LPS（100马克杯/千克，腹膜内注射）治疗，将卵巢切除的雌性后代致敏并在成年后期用OVA攻击。在这些75日龄的幼犬中评估了支气管肺泡灌洗液（BAL），外周血，骨髓白细胞和被动性皮肤过敏反应。主要发现：OVA激发后，经NaCl处理的OVA致敏幼崽的BAL中白细胞增多。当母亲在怀孕初期接受一次LPS注射时，这种增加就会减弱。因此，LPS产前治疗导致（1）BAL细胞总数的总和差异（巨噬细胞，嗜中性粒细胞，嗜酸性粒细胞和淋巴细胞）增加降低; （2）外周血中总，单核和多形核细胞数量增加; （3）骨髓细胞或被动皮肤过敏反应无差异。意义：总之，产前用LPS治疗的雌性幼犬对实验性哮喘的反应减弱。我们观察到免疫细胞从外周血向肺部的迁移减少，对骨髓细胞或抗体的产生没有影响。有研究表明，在胎儿早期生命中，诸如暴露于LPS等炎症事件可以减轻肺部的过敏性炎症，这是哮喘的常见症状。

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