Mothers and Babies Research Centre, Hunter Medical Research Institute, University of Newcastle, Newcastle, NSW, Australia.
Placenta. 2011 Jun;32(6):454-61. doi: 10.1016/j.placenta.2011.03.004. Epub 2011 Mar 31.
The mechanisms that contribute to adverse outcomes for the neonate in pregnancies complicated by asthma may be mediated via changes in placental immune function. This study was designed to determine whether the presence of maternal asthma during pregnancy alters the placental pro-inflammatory immune response in vitro. A prospective cohort study of women with asthma (n = 22) and control (n = 11) subjects had placentae collected immediately after delivery. Placental explants were exposed to an immune challenge, lipopolysaccharide, in the presence and absence of cortisol in vitro. Cytokines, glucocorticoid receptor α (GR α) and p38 MAPK protein were measured. Placentae of control pregnancies had an increase in pro-inflammatory cytokine production over a 24 h period. Placentae from pregnancies complicated by maternal asthma had a reduced pro-inflammatory cytokine response to an immune challenge relative to the controls especially in relation to the production of interleukin (IL)-1β and TNFα regardless of fetal sex. Cortisol inhibition of placental cytokine production was dependent on timing of exposure, fetal sex and presence and absence of asthma. GRα and p38 MAPK protein expression did not appear to contribute to differences in response to endotoxin or cortisol. Maternal asthma during pregnancy induces a hyposensitive inflammatory state in the placenta which is regulated by cortisol in a sexually dimorphic manner.
导致妊娠合并哮喘的新生儿不良结局的机制可能通过胎盘免疫功能的改变来介导。本研究旨在确定妊娠期间母亲哮喘的存在是否会改变体外胎盘的促炎免疫反应。对 22 例哮喘（n=22）和 11 例对照（n=11）孕妇进行前瞻性队列研究，在分娩后立即采集胎盘。胎盘外植体在体外暴露于脂多糖的免疫挑战中，同时存在和不存在皮质醇。测量细胞因子、糖皮质激素受体α（GRα）和 p38 MAPK 蛋白。与对照组相比，妊娠合并母亲哮喘的胎盘在 24 小时内产生促炎细胞因子的能力降低，特别是与白细胞介素（IL）-1β和 TNFα的产生有关，而与胎儿性别无关。皮质醇对胎盘细胞因子产生的抑制作用取决于暴露的时间、胎儿性别以及是否存在哮喘。GRα和 p38 MAPK 蛋白表达似乎并未导致对内毒素或皮质醇的反应存在差异。妊娠期间母亲哮喘会导致胎盘呈低敏性炎症状态，这种状态受皮质醇的影响呈性别二态性调节。
