Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae

<p>The trophoblast cells are in direct contact with endometrial tissues throughout gestation, playing important early roles in implantation and placentation. The physiologic significance and the operating mechanisms involved in probable altered trophoblast functions following <i>Chlamydi...

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Main Author: Anthony A. Azenabor, Patrick Kennedy, Salvatore Balistreri
Format: Article
Language:English
Published: Ivyspring International Publisher 2007-01-01
Series:International Journal of Medical Sciences
Online Access:http://www.medsci.org/v04p0223.htm
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spelling doaj-8c4ca71d3f3a43089adf0de8ab38382f2020-11-25T01:02:27ZengIvyspring International PublisherInternational Journal of Medical Sciences1449-19072007-01-0144223231Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelaeAnthony A. Azenabor, Patrick Kennedy, Salvatore Balistreri<p>The trophoblast cells are in direct contact with endometrial tissues throughout gestation, playing important early roles in implantation and placentation. The physiologic significance and the operating mechanisms involved in probable altered trophoblast functions following <i>Chlamydia trachomatis</i> infection were investigated to determine if <i>C. trachomatis</i> initiates productive infection in trophoblast, effects of such event on the biosynthesis of cholesterol and its derivatives estrogen and progesterone; and the regulator of the biosynthesis of these hormones, human chorionic gonadotropin. <i>Chlamydia trachomatis</i> exhibited productive infection in trophoblast typified by inclusion formation observed when chlamydia elementary bodies were harvested from trophoblast and titrated onto HEp-2 cells. Assessment of the status of <i>C. trachomatis</i> in trophoblast showed a relative increase in protein of HSP-60 compared with MOMP, features suggestive of chlamydial chronicity. There was a decrease in cellular cholesterol of chlamydia infected trophoblast and a down regulation of HMG-CoA reductase. The levels of estrogen and progesterone were decreased, while the expression of aromatase and adrenodoxin reductase was up regulated. Also, there was a decrease in human chorionic gonadotropin expression. The implications of these findings are that <i>C. trachomatis</i> infection of trophoblast may compromise cellular cholesterol biosynthesis, thus depleting the substrate pool for estrogen and progesterone synthesis. This defect may impair trophoblast functions of implantation and placentation, and consequently affect pregnancy sequelae.</p>http://www.medsci.org/v04p0223.htm
collection DOAJ
language English
format Article
sources DOAJ
author Anthony A. Azenabor, Patrick Kennedy, Salvatore Balistreri
spellingShingle Anthony A. Azenabor, Patrick Kennedy, Salvatore Balistreri
Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae
International Journal of Medical Sciences
author_facet Anthony A. Azenabor, Patrick Kennedy, Salvatore Balistreri
author_sort Anthony A. Azenabor, Patrick Kennedy, Salvatore Balistreri
title Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae
title_short Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae
title_full Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae
title_fullStr Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae
title_full_unstemmed Chlamydia trachomatis Infection of Human Trophoblast Alters Estrogen and Progesterone Biosynthesis: an insight into role of infection in pregnancy sequelae
title_sort chlamydia trachomatis infection of human trophoblast alters estrogen and progesterone biosynthesis: an insight into role of infection in pregnancy sequelae
publisher Ivyspring International Publisher
series International Journal of Medical Sciences
issn 1449-1907
publishDate 2007-01-01
description <p>The trophoblast cells are in direct contact with endometrial tissues throughout gestation, playing important early roles in implantation and placentation. The physiologic significance and the operating mechanisms involved in probable altered trophoblast functions following <i>Chlamydia trachomatis</i> infection were investigated to determine if <i>C. trachomatis</i> initiates productive infection in trophoblast, effects of such event on the biosynthesis of cholesterol and its derivatives estrogen and progesterone; and the regulator of the biosynthesis of these hormones, human chorionic gonadotropin. <i>Chlamydia trachomatis</i> exhibited productive infection in trophoblast typified by inclusion formation observed when chlamydia elementary bodies were harvested from trophoblast and titrated onto HEp-2 cells. Assessment of the status of <i>C. trachomatis</i> in trophoblast showed a relative increase in protein of HSP-60 compared with MOMP, features suggestive of chlamydial chronicity. There was a decrease in cellular cholesterol of chlamydia infected trophoblast and a down regulation of HMG-CoA reductase. The levels of estrogen and progesterone were decreased, while the expression of aromatase and adrenodoxin reductase was up regulated. Also, there was a decrease in human chorionic gonadotropin expression. The implications of these findings are that <i>C. trachomatis</i> infection of trophoblast may compromise cellular cholesterol biosynthesis, thus depleting the substrate pool for estrogen and progesterone synthesis. This defect may impair trophoblast functions of implantation and placentation, and consequently affect pregnancy sequelae.</p>
url http://www.medsci.org/v04p0223.htm
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