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

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*

*Corresponding author for this work

Research output: Contribution to journalArticle (Academic Journal)peer-review

17 Citations (Scopus)
316 Downloads (Pure)


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.

Original languageEnglish
Article number2001
JournalScientific Reports
Issue number1
Early online date17 May 2017
Publication statusE-pub ahead of print - 17 May 2017


  • Infectious diseases
  • innate immunity
  • reproductive biology


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