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Trophoblast-microbiome interaction: a new paradigm on immune regulation

Authors
 Gil Mor ; Ja-Young Kwon 
Citation
 American Journal of Obstetrics and Gynecology, Vol.213(4 Suppl.) : S131~S137, 2015 
Journal Title
 American Journal of Obstetrics and Gynecology 
ISSN
 0002-9378 
Issue Date
2015
Abstract
The immunologic paradigm of pregnancy led to the conceptualization of pregnancy as an organ transplant that requires, for its success, suppression of the maternal immune system. Growing scientific evidence suggests that in many ways the placenta functions as a tumor rather than a transplant and the immune regulation of the maternal-fetal interface is the result of the coordinated interaction between all its cellular components, including bacteria. Examining the role of microbiota in reproduction is in its infancy, but there is growing literature that supports its relevance. We discuss a potential normal function of bacteria in the establishment of immune tolerance and compelling evidence that a viral infection might be the underlying cause of perturbation of homeostasis. There is compelling evidence that many infectious diseases of human beings are caused by >1 microorganism and are defined as polymicrobial infections. We propose that pregnancy complications, such as preterm birth, are the result of polymicrobial infections. We examine the potential cellular and molecular mechanisms by which a viral infection of the placenta might disrupt the normal interaction between the cellular component of the implantation site and bacteria. As we better understand the normal homeostasis among the maternal immune system, placenta, and commensal, we will be able to elucidate pathogenic conditions and design better approaches to treat pregnancy complications associated with infection.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/141364
DOI
10.1016/j.ajog.2015.06.039
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Obstetrics & Gynecology
Yonsei Authors
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Link
 http://www.sciencedirect.com/science/article/pii/S0002937815006523
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