血源性:母亲血液中的细菌成分影响胎儿发育。

Allister J Loughran, Elaine I Tuomanen
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引用次数: 3

摘要

母亲在怀孕期间的细菌或病毒感染可以穿过胎盘,主动感染胎儿。然而,特别是对于细菌,更常见的是母亲经历感染,可以治疗没有明显的胎儿感染。在这种情况下,人们对胎儿发育的风险知之甚少,特别是在神经发育方面。本研究重点回顾了最近的研究结果,表明母亲感染期间产生的细菌成分可以穿过胎盘,激活胎儿先天免疫系统,导致大脑发育过程的变化,并随后发展为产后认知障碍。细菌细胞壁是一种普遍存在的细菌PAMP(病原体相关分子模式),已知通过刺激TLR2激活炎症。在抗生素治疗期间,细胞壁从细菌中释放出来,新的研究表明,暴露于母体细胞壁的胚胎以TLR2依赖的方式表现出神经元前体细胞的异常增殖。这种增生增加了皮质板的神经元密度,改变了大脑结构。虽然没有胎儿死亡,但随后的认知发育明显受损。这个模型系统表明,母亲的细菌感染及其治疗可以影响胎儿的大脑发育,需要更多的了解,以潜在地消除自闭症等认知障碍的风险因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Blood borne: bacterial components in mother's blood influence fetal development.

Bacterial or viral infection of the mother during the course of pregnancy can cross the placenta and actively infect the fetus. However, especially for bacteria, it is more common for mothers to experience an infection that can be treated without overt fetal infection. In this setting, it is less well understood what the risk to fetal development is, particularly in terms of neurological development. This research highlight reviews recent findings indicating that bacterial components generated during infection of the mother can cross the placenta and activate the fetal innate immune system resulting in changes in the course of brain development and subsequent progression to postnatal cognitive disorders. Bacterial cell wall is a ubiquitous bacterial PAMP (pathogen-associated molecular pattern) known to activate inflammation through the stimulation of TLR2. Cell wall is released from bacteria during antibiotic treatment and new work shows that embryos exposed to cell wall from the mother demonstrate anomalous proliferation of neuronal precursor cells in a TLR2 dependent manner. Such proliferation increases the neuronal density of the cortical plate and alters brain architecture. Although there is no fetal death, subsequent cognitive development is significantly impaired. This model system suggests that bacterial infection of the mother and its treatment can impact fetal brain development and requires greater understanding to potentially eliminate a risk factor for cognitive disorders such as autism.

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