Inflammation-induced preterm birth alters neuronal morphology in the mouse fetal brain.
Inflammation-induced preterm birth alters neuronal morphology in the mouse fetal brain.
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DOI：
10.1002/jnr.22368
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发表时间：
2010-07
影响因子：
4.2
通讯作者：
Elovitz MA
中科院分区：
文献类型：
--
作者：
Burd I;Bentz AI;Chai J;Gonzalez J;Monnerie H;Le Roux PD;Cohen AS;Yudkoff M;Elovitz MA
不良神经系统结局是早产儿长期发病的主要原因。为了研究分娩和炎症对胎儿大脑的影响，我们利用了两种早产体内小鼠模型。为了模拟人类最常见的早产情况，我们通过宫内输注脂多糖（LPS）建立了小鼠子宫内炎症模型。为了研究分娩对未成熟胎儿大脑的影响，在没有炎症的情况下，我们使用 RU486 建立了非感染性早产模型。使用 ELISA 比较两个模型之间羊水中的促炎细胞因子（IL-10、IL-1β、IL-6 和 TNF-α）以及母体血清和羊水中的炎症生物标志物。在两个模型的整个胎儿大脑中评估促炎细胞因子的表达。从不同的模型和对照中建立来自胎儿皮质的原代神经元培养物，以比较神经元形态。只有宫内炎症模型导致母体血清和羊水中炎症生物标志物升高。暴露于炎症诱发的早产（而非非感染性早产）也会导致整个胎儿大脑中细胞因子 mRNA 的增加以及胎儿神经元形态的破坏。特别是，微管相关蛋白 2 (MAP2) 染色减少，树突数量减少（P < 0.001，组间方差分析）。这些结果表明炎症诱导的早产而不是早产过程可能导致神经炎症并改变胎儿神经元形态。
Adverse neurological outcome is a major cause of long-term morbidity in ex-preterm children. To investigate the effect of parturition and inflammation on the fetal brain, we utilized two in vivo mouse models of preterm birth. To mimic the most common human scenario of preterm birth, we used a mouse model of intrauterine inflammation by intrauterine infusion of lipopolysaccharide (LPS). To investigate the effect of parturition on the immature fetal brain, in the absence of inflammation, we used a non-infectious model of preterm birth by administering RU486. Pro-inflammatory cytokines (IL-10, IL-1β, IL-6 and TNF-α) in amniotic fluid and inflammatory biomarkers in maternal serum and amniotic fluid were compared between the two models using ELISA. Pro-inflammatory cytokine expression was evaluated in the whole fetal brains from the two models. Primary neuronal cultures from the fetal cortex were established from the different models and controls in order to compare the neuronal morphology. Only the intrauterine inflammation model resulted in an elevation of inflammatory biomarkers in the maternal serum and amniotic fluid. Exposure to inflammation-induced preterm birth, but not non-infectious preterm birth, also resulted in an increase in cytokine mRNA in whole fetal brain and in disrupted fetal neuronal morphology. In particular, Microtubule-associated protein 2 (MAP2) staining was decreased and the number of dendrites was reduced (P < 0.001, ANOVA between groups). These results suggest that inflammation-induced preterm birth and not the process of preterm birth may result in neuroinflammation and alter fetal neuronal morphology.
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影响因子：
9.8
作者：
Elovitz, MA;Mrinalini, C
通讯作者：
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影响因子：
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作者：
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作者：
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DOI：
10.1111/j.1471-0528.2006.01118.x
发表时间：
2006-12-01
影响因子：
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作者：
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通讯作者：
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