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免疫耐受、妊娠与子痫前期:精液微生物及父亲的作用

Immunological Tolerance, Pregnancy, and Preeclampsia: The Roles of Semen Microbes and the Father.

作者信息

Kenny Louise C, Kell Douglas B

机构信息

The Irish Centre for Fetal and Neonatal Translational Research (INFANT), University College Cork, Cork, Ireland.

Department of Obstetrics and Gynecology, University College Cork, Cork, Ireland.

出版信息

Front Med (Lausanne). 2018 Jan 4;4:239. doi: 10.3389/fmed.2017.00239. eCollection 2017.

DOI:10.3389/fmed.2017.00239
PMID:29354635
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5758600/
Abstract

Although it is widely considered, in many cases, to involve two separable stages (poor placentation followed by oxidative stress/inflammation), the precise originating causes of preeclampsia (PE) remain elusive. We have previously brought together some of the considerable evidence that a (dormant) microbial component is commonly a significant part of its etiology. However, apart from recognizing, consistent with this view, that the many inflammatory markers of PE are also increased in infection, we had little to say about immunity, whether innate or adaptive. In addition, we focused on the gut, oral and female urinary tract microbiomes as the main sources of the infection. We here marshall further evidence for an infectious component in PE, focusing on the immunological tolerance characteristic of pregnancy, and the well-established fact that increased exposure to the father's semen assists this immunological tolerance. As well as these benefits, however, semen is not sterile, microbial tolerance mechanisms may exist, and we also review the evidence that semen may be responsible for inoculating the developing conceptus (and maybe the placenta) with microbes, not all of which are benign. It is suggested that when they are not, this may be a significant cause of PE. A variety of epidemiological and other evidence is entirely consistent with this, not least correlations between semen infection, infertility and PE. Our view also leads to a series of other, testable predictions. Overall, we argue for a significant paternal role in the development of PE through microbial infection of the mother insemination.

摘要

尽管在许多情况下,子痫前期(PE)被广泛认为涉及两个可分离的阶段(胎盘形成不良随后是氧化应激/炎症),但其确切的起源原因仍然难以捉摸。我们之前汇集了一些重要证据,表明(潜伏的)微生物成分通常是其病因的重要组成部分。然而,除了认识到与这种观点一致的是,PE的许多炎症标志物在感染中也会增加之外,我们对于免疫,无论是先天免疫还是适应性免疫,几乎没有提及。此外,我们将肠道、口腔和女性泌尿道微生物群视为感染的主要来源。我们在此汇集了更多关于PE中感染成分的证据,重点关注妊娠的免疫耐受特性,以及增加接触父亲精液有助于这种免疫耐受这一既定事实。然而,除了这些益处之外,精液并非无菌,可能存在微生物耐受机制,我们还回顾了精液可能负责将微生物接种到发育中的胚胎(也许还有胎盘)的证据,并非所有这些微生物都是无害的。有人认为,当它们有害时,这可能是PE的一个重要原因。各种流行病学和其他证据完全与此一致,尤其是精液感染、不孕与PE之间的相关性。我们的观点还导致了一系列其他可检验的预测。总体而言,我们认为父亲通过母亲授精时的微生物感染在PE的发生发展中起着重要作用。

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