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Unique maternal immune and functional microbial profiles during prenatal stress
bioRxiv - Immunology Pub Date : 2020-05-29 , DOI: 10.1101/2020.05.26.116574
Adrienne M. Antonson , Morgan V. Evans , Jeffrey D. Galley , Helen J. Chen , Therese A. Rajesekera , Sydney M. Lammers , Vanessa L. Hale , Michael T. Bailey , Tamar L. Gur

Maternal stress during pregnancy is widespread and stress-induced fetal neuroinflammation is thought to derive from a disruption in intrauterine immune homeostasis, though the exact origins are incompletely defined. We aimed to identify divergent immune and microbial metagenome profiles of stressed gestating mice that may underlie detrimental inflammatory signaling at the maternal-fetal interface. In response to stress, maternal glucocorticoid circuit activation corresponded with diminished spleen mass and IL-1β production, reflecting systemic immunosuppression. At the maternal-fetal interface, density of placental mononuclear leukocytes decreased with stress. Yet maternal whole blood leukocyte analysis indicated monocytosis and classical M1 phenotypic shifts. Genome-resolved microbial metagenomic analyses revealed reductions in genes, microbial strains, and metabolic pathways in stressed dams that are primarily associated with pro-inflammatory function. Overall, these data indicate that stress disrupts maternal immunological and microbial regulation during pregnancy, characterized by concurrent anti- and pro-inflammatory signatures, which may displace immune equilibrium at the maternal-fetal interface.

中文翻译:

产前压力期间独特的母体免疫和功能微生物谱

怀孕期间的孕产妇压力普遍存在,并且应力诱发的胎儿神经炎症被认为是由于子宫内免疫稳态的破坏而引起的,尽管确切的来源尚未完全确定。我们旨在鉴定应激妊娠小鼠的不同免疫和微生物基因组图谱,这些谱图可能是母胎界面有害炎症信号的基础。响应压力,母亲的糖皮质激素回路激活与脾脏质量和IL-1β产生减少相对应,反映了系统性免疫抑制。在母胎界面,胎盘单核白细胞的密度随着压力而降低。然而,孕妇全血白细胞分析显示单核细胞增多和经典的M1表型转移。基因组分辨的微生物宏基因组学分析显示基因减少,微生物菌株以及应激水坝中的代谢途径,这些途径主要与促炎功能有关。总体而言,这些数据表明,压力在怀孕期间破坏了母体的免疫学和微生物调节,其特征是同时存在抗炎和促炎性信号,这可能会取代母体-胎儿界面的免疫平衡。
更新日期:2020-05-29
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