Prenatal programing: At the intersection of maternal stress and immune activation

被引:107
作者
Howerton, Christopher L. [1 ]
Bale, Tracy L. [1 ]
机构
[1] Univ Penn, Sch Vet Med, Neurosci Ctr, Dept Anim Biol, Philadelphia, PA 19104 USA
基金
美国国家卫生研究院;
关键词
Maternal stress; Immune-activation; Fetal programing; Neurodevelopment; Epigenetic; Sex; Placenta; Glucocorticoids; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-2; BETA-HYDROXYSTEROID DEHYDROGENASE; PITUITARY-ADRENAL AXIS; GLUCOCORTICOID EXPOSURE; PSYCHOLOGICAL STRESS; PREPULSE INHIBITION; GENE-EXPRESSION; CYTOKINE LEVELS; SEX-DIFFERENCES; BIRTH-WEIGHT;
D O I
10.1016/j.yhbeh.2012.03.007
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
This article is part of a Special Issue "Neuroendocrine-Immune Axis in Health and Disease." Exposure to prenatal insults such as maternal stress and pathogenic infections has been associated with an increased risk for neurodevelopmental disorders. The mechanisms by which these programing events occur likely involve complex interactions between the maternal hormonal milieu, the placenta, and the developing fetus, in addition to compounding factors such as fetal sex and gestational stage of development. Despite the diverse biological processes involved, examination of common pathways in maternal stress and immune activation offers intriguing possibilities for elucidation of mechanistic insight. Further, the endocrine and sex-specific placenta is a tissue poised to be a key mediator in fetal programing, located at the intersection of the maternal and embryonic environments. In this review, we will discuss the potential shared mechanisms of maternal stress and immune pathway activation, with a particular focus on the important contribution and role of the placenta. This article is part of a Special Issue entitled (The Neuroendocrine-Immune). (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:237 / 242
页数:6
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