Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production

Eugenia De La Torre, Melissa J. Mulla, Andrew G. Yu, Seung Joon Lee, Paula B. Kavathas, Vikki M. Abrahams

Research output: Contribution to journalArticle

24 Scopus citations

Abstract

It is well established that intrauterine infections can pose a threat to pregnancy by gaining access to the placenta and fetus, and clinical studies have strongly linked bacterial infections with preterm labor. Although Chlamydia trachomatis (Ct) can infect the placenta and decidua, little is known about its effects on trophoblast cell immune function. We have demonstrated that Ct infects trophoblast cells to form inclusions and completes the life cycle within these cells by generating infectious elementary bodies. Moreover, infection with Ct leads to differential modulation of the trophoblast cell's production of cytokines and chemokines. Using two human first trimester trophoblast cell lines, Sw.71 and H8, the most striking feature we found was that Ct infection results in a strong induction of IL-1β secretion and a concomitant reduction in MCP-1 (CCL2) production in both cell lines. In addition, we have found that Ct infection of the trophoblast results in the cleavage and degradation of NF-κB p65. These findings suggest that the effect of a Chlamydia infection on trophoblast secretion of chemokines and cytokines involves both activation of innate immune receptors expressed by the trophoblast and virulence factors secreted into the trophoblast by the bacteria. Such altered trophoblast innate immune responses may have a profound impact on the microenvironment of the maternal-fetal interface and this could influence pregnancy outcome.

Original languageEnglish (US)
Pages (from-to)3735-3745
Number of pages11
JournalJournal of Immunology
Volume182
Issue number6
DOIs
StatePublished - Mar 15 2009
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production'. Together they form a unique fingerprint.

  • Cite this

    De La Torre, E., Mulla, M. J., Yu, A. G., Lee, S. J., Kavathas, P. B., & Abrahams, V. M. (2009). Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production. Journal of Immunology, 182(6), 3735-3745. https://doi.org/10.4049/jimmunol.0800764