Prenatal inflammation and lung development.
Prenatal inflammation and lung development.
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DOI：
10.1016/j.siny.2008.08.011
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发表时间：
2009-02
影响因子：
3
通讯作者：
Jobe, Alan H.
中科院分区：
文献类型：
--
作者：
Kramer, Boris W.;Kallapur, Suhas;Newnham, John;Jobe, Alan H.
极低出生体重儿产前暴露于慢性无痛性绒毛膜炎（包括支原体和脲原体）是常见的。绒毛膜炎与呼吸窘迫综合征（RDS）或支气管肺发育不良（BPD）的风险变化不一致，可能是因为绒毛膜炎的诊断不能量化胎儿暴露于感染和炎症的程度或持续时间。产前暴露与出生后肺部疾病之间的相关性也被RDS和BPD诊断的不精确所混淆。在动物模型中，由促炎介质或活脲原体引起的绒毛膜炎诱导肺成熟，但也引起肺泡简化和血管损伤。羊膜内给予内毒素还调节胎儿先天免疫系统，导致单核细胞成熟为肺泡巨噬细胞，并根据暴露史诱导或麻痹炎症反应。产前炎症可对胎儿肺和随后的免疫反应产生深远影响。
Prenatal exposure of very low birth weight infants to chronic indolent chorioamnionitis with organisms such as mycoplasma and ureaplasma is frequent. Chorioamnionitis is inconsistently associated with changed risks of respiratory distress syndrome (RDS) or bronchopulmonary dysplasia (BPD), probably because the diagnosis of chorioamnionitis does not quantify the extent or duration of the fetal exposures to infection and inflammation. The correlations between prenatal exposures and postnatal lung disease also are confounded by the imprecision of the diagnoses of RDS and BPD. In animal models, chorioamnionitis caused by pro-inflammatory mediators or live ureaplasma induces lung maturation, but also causes alveolar simplification and vascular injury. Intra-amniotic endotoxin administration also modulates the fetal innate immune system, resulting in maturation of monocytes to alveolar macrophages and the induction or paralysis of inflammatory responses depending on exposure history. Prenatal inflammation can have profound effects on the fetal lung and subsequent immune responses.
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DOI：
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10.1152/ajplung.2001.280.3.l527
发表时间：
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