Department of Psychiatry, University of Iowa Carver College of Medicine, 1330 PBDB, 169 Newton Rd., Iowa City, IA, 52246, USA.
Interdisciplinary Graduate Program in Neuroscience, University of Iowa, 356 Medical Research Center, Iowa City, IA, 52242, USA.
J Neuroinflammation. 2018 Feb 16;15(1):44. doi: 10.1186/s12974-018-1079-7.
Maternal stress during pregnancy is associated with an increased risk of psychopathology in offspring. Resident immune cells of the brain, microglia, may be mediators of prenatal stress and altered neurodevelopment. Here, we demonstrate that neither the exogenous pro-inflammatory cytokine, interleukin-1β (IL-1β), nor the glucocorticoid hormone, corticosterone, recapitulated the full effects of prenatal stress on the morphology of microglial cells in the cortical plate of embryonic mice; IL-1β effects showed greater similarity to prenatal stress effects on microglia. Unexpectedly, oil vehicle alone, which has antioxidant properties, moderated the effects of prenatal stress on microglia. Microglia changes with prenatal stress were also sensitive to the antioxidant, N-acetylcysteine, suggesting redox dysregulation as a mechanism of prenatal stress.
孕期母体应激与后代精神病理学风险增加有关。大脑常驻免疫细胞——小胶质细胞，可能是产前应激和神经发育改变的中介。在这里，我们证明外源性促炎细胞因子白细胞介素-1β (IL-1β) 和糖皮质激素皮质酮都不能完全模拟产前应激对胚胎期小鼠皮质板中小胶质细胞形态的影响；IL-1β 的作用与产前应激对小胶质细胞的作用更相似。出乎意料的是，具有抗氧化特性的油载体本身就可以调节产前应激对小胶质细胞的作用。产前应激引起的小胶质细胞变化对抗氧化剂 N-乙酰半胱氨酸也很敏感，这表明氧化还原失调是产前应激的一种机制。
