Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release

Abstract Miscarriage affects ~20% of pregnancies and maternal infections account for ~15% of early miscarriages. Chlamydia trachomatis (Ct) has been associated with miscarriage but the underlying mechanisms are unknown. Successful implantation requires endometrial stromal cell (ESC) decidualisation....

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Autores principales:	Sevi Giakoumelou, Nick Wheelhouse, Jeremy Brown, Jean Wade, Ioannis Simitsidellis, Douglas Gibson, Philippa T. K. Saunders, Patrick Horner, Gary Entrican, Sarah E. M. Howie, Andrew W. Horne
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/a46600d160d7406588f985428bf14742
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spelling	oai:doaj.org-article:a46600d160d7406588f985428bf147422021-12-02T16:06:28ZChlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release10.1038/s41598-017-02223-z2045-2322https://doaj.org/article/a46600d160d7406588f985428bf147422017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02223-zhttps://doaj.org/toc/2045-2322Abstract Miscarriage affects ~20% of pregnancies and maternal infections account for ~15% of early miscarriages. Chlamydia trachomatis (Ct) has been associated with miscarriage but the underlying mechanisms are unknown. Successful implantation requires endometrial stromal cell (ESC) decidualisation. Maintenance of pregnancy requires angiogenesis, establishment of the correct cellular milieu and trophoblast invasion, all of which involve the action of chemokines. Our objective was to determine whether Ct infection impacts upon ESC decidualisation and chemokine secretion. Human primary ESC were decidualised in-vitro, infected with Ct serovar E, and changes in expression of genes of interest were measured using RT-PCR, proteomic array and ELISA. We demonstrate for the first time that Ct can infect and proliferate in ESC. Expression of the decidualisation marker prolactin was decreased in Ct-infected ESC at both mRNA and protein levels. Ct infection altered the chemokine profile of decidualised ESC as shown by proteomic array. Chemokines CXCL12 and CXCL16, important for trophoblast invasion, were analysed further and expression was reduced in infected decidualised cells at mRNA and protein levels. Our data indicate that Ct infection of ESC impairs decidualisation and alters chemokine release. These findings at least partially explain how Ct infection could result in adverse pregnancy outcomes.Sevi GiakoumelouNick WheelhouseJeremy BrownJean WadeIoannis SimitsidellisDouglas GibsonPhilippa T. K. SaundersPatrick HornerGary EntricanSarah E. M. HowieAndrew W. HorneNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Sevi Giakoumelou Nick Wheelhouse Jeremy Brown Jean Wade Ioannis Simitsidellis Douglas Gibson Philippa T. K. Saunders Patrick Horner Gary Entrican Sarah E. M. Howie Andrew W. Horne Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
description	Abstract Miscarriage affects ~20% of pregnancies and maternal infections account for ~15% of early miscarriages. Chlamydia trachomatis (Ct) has been associated with miscarriage but the underlying mechanisms are unknown. Successful implantation requires endometrial stromal cell (ESC) decidualisation. Maintenance of pregnancy requires angiogenesis, establishment of the correct cellular milieu and trophoblast invasion, all of which involve the action of chemokines. Our objective was to determine whether Ct infection impacts upon ESC decidualisation and chemokine secretion. Human primary ESC were decidualised in-vitro, infected with Ct serovar E, and changes in expression of genes of interest were measured using RT-PCR, proteomic array and ELISA. We demonstrate for the first time that Ct can infect and proliferate in ESC. Expression of the decidualisation marker prolactin was decreased in Ct-infected ESC at both mRNA and protein levels. Ct infection altered the chemokine profile of decidualised ESC as shown by proteomic array. Chemokines CXCL12 and CXCL16, important for trophoblast invasion, were analysed further and expression was reduced in infected decidualised cells at mRNA and protein levels. Our data indicate that Ct infection of ESC impairs decidualisation and alters chemokine release. These findings at least partially explain how Ct infection could result in adverse pregnancy outcomes.
format	article
author	Sevi Giakoumelou Nick Wheelhouse Jeremy Brown Jean Wade Ioannis Simitsidellis Douglas Gibson Philippa T. K. Saunders Patrick Horner Gary Entrican Sarah E. M. Howie Andrew W. Horne
author_facet	Sevi Giakoumelou Nick Wheelhouse Jeremy Brown Jean Wade Ioannis Simitsidellis Douglas Gibson Philippa T. K. Saunders Patrick Horner Gary Entrican Sarah E. M. Howie Andrew W. Horne
author_sort	Sevi Giakoumelou
title	Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
title_short	Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
title_full	Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
title_fullStr	Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
title_full_unstemmed	Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
title_sort	chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/a46600d160d7406588f985428bf14742
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Chlamydia trachomatis infection of human endometrial stromal cells induces defective decidualisation and chemokine release

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