Causes for spontaneous abortion: What the bugs 'gut' to do with it?

Causes for spontaneous abortion: What the bugs 'gut' to do with it?
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DOI:
10.1016/j.biocel.2008.04.019
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发表时间:
2008-01-01
影响因子:
4
通讯作者:
Arck, Petra
Arck, Petra
中科院分区:
生物学2区
文献类型:
--
作者:
Friebe, Astrid;Arck, Petra

文献摘要

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自然流产是人类最常见的不良妊娠结局,占所有公认妊娠的 15-20%。长期以来,高心理社会压力感知被认为是对妊娠维持的威胁,并且越来越多的证据表明压力会影响母亲对妊娠的适应,从而阻碍胎儿母亲的耐受性。本综述重点关注微生物产物在应激诱导的信号级联中的作用,将内源微生物群的不平衡与免疫激活和妊娠丢失联系起来。应激信号级联利用脂多糖 (LPS) 的存在,脂多糖 (LPS) 通过 Toll 样受体 4 充当危险信号。从生理学角度来看,肠道菌群提供了内源性 LPS 的来源,即在应激反应期间,小鼠的心理社会应激挑战增强了胃肠道通透性和肠道细菌摄取。显然,这些新颖的见解不仅加深了我们对应激反应级联机制的理解,而且还启动了治疗干预策略的复兴,旨在通过益生菌调节肠道菌群。反过来,肠道屏障功能可能会得到增强,免疫耐受的介质可能会得到恢复,即在繁殖的情况下。 (C) 2008 Elsevier Ltd. 保留所有权利。
Spontaneous miscarriage is the most common adverse pregnancy outcome in humans and occurs in 15-20% of all recognized pregnancies. High psychosocial stress perception has long been recognized as a threat to pregnancy maintenance and accumulating evidence supports that stress affects maternal adaptation to pregnancy and subsequently impedes fetomaternal tolerance. This review strongly focuses on the role of microbial products within the stress-induced signalling cascade, linking the disequilibrium of the endogenous microflora to immune activation and pregnancy loss. The stress signalling cascade utilizes the presence of lipopolysaccharide (LPS), which acts as a danger signal via Toll like receptor 4. Physiologically, the intestinal microflora provides a source for endogenous LPS, i.e. during the stress response, and psychosocial stress challenge in mice enhances the gastrointestinal permeability and bacterial uptake from the gut. Clearly, these novel insights not only deepen our understanding of mechanisms involved in the stress response cascade, but also initiate a renaissance of therapeutic intervention strategies, aiming to modulate the intestinal flora by probiotic bacteria. In turn, intestinal barrier function may be enhanced and mediators of immune tolerance may be restored, i.e. in the context of reproduction. (C) 2008 Elsevier Ltd. All rights reserved.