4.4 Review

Placental microbial-metabolite profiles and inflammatory mechanisms associated with preterm birth

期刊

JOURNAL OF CLINICAL PATHOLOGY
卷 74, 期 1, 页码 10-18

出版社

BMJ PUBLISHING GROUP
DOI: 10.1136/jclinpath-2020-206536

关键词

maternal-fetal; placenta; pregnancy; microbial pathogenic; immunopathology

资金

  1. National Institute for Health Research (NIHR) [17/63/26]
  2. National Institutes of Health Research (NIHR) [17/63/26] Funding Source: National Institutes of Health Research (NIHR)

向作者/读者索取更多资源

This article discusses the potential significance of the placental microbiome and microbiome-metabolite interactions in immune responses and pregnancy outcomes, with a focus on pathomechanisms of placental inflammatory responses and predictive markers for preterm birth. It also provides an overview of the current understanding of the placental microbiome and metabolome in human pregnancy, evaluating the evidence for its existence and its role in fetomaternal inflammatory responses leading to preterm birth.
There is growing emphasis on the potential significance of the placental microbiome and microbiome-metabolite interactions in immune responses and subsequent pregnancy outcome, especially in relation to preterm birth (PTB). This review discusses in detail the pathomechanisms of placental inflammatory responses and the resultant maternal-fetal allograft rejection in both microbial-induced and sterile conditions. It also highlights some potential placental-associated predictive markers of PTB for future investigation. The existence of a placental microbiome remains debatable. Therefore, an overview of our current understanding of the state and role of the placental microbiome (if it exists) and metabolome in human pregnancy is also provided. We critical evaluate the evidence for a placental microbiome, discuss its functional capacity through the elaborated metabolic products and also describe the consequent and more established fetomaternal inflammatory responses that stimulate the pathway to preterm premature rupture of membranes, preterm labour and spontaneous PTB.

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