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Chlamydia trachomatis Infection Modulates Trophoblast Cytokine/Chemokine Production¹

Eugenia de la Torre^2,*, Melissa J. Mulla, Andrew G. Yu, Seung-Joon Lee^3,*, Paula B. Kavathas^4,5,* and Vikki M. Abrahams^4,5,

^* Department of Laboratory Medicine, Immunobiology and Genetics and Department of Obstetrics, Gynecology & Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06520

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-B 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.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This study was supported, in part, by Grants R01049571 (to P.B.K.) and R01HD049446 (to V.M.A.) from the National Institutes of Health.

² Current address: Campus de Bellaterra, edifici CReSA, 08193 Bellaterra, Barcelona, Spain.

³ Current address: Department of Internal Medicine, Kangwon National University School of Medicine, 1 Kangwondaehak-Gil, Chuncheon, Kangwon-Do, South Korea 200-701.

⁴ This work was a collaboration between two principal investigators (P.B.K. and V.M.A.), who made equal contributions to this project.

⁵ Address correspondence and reprint requests to Dr. Vikki M. Abrahams, Department of Obstetrics, Gynecology & Reproductive Sciences and Dr. Paula B. Kavathas, Department of Laboratory Medicine, Immunobiology and Genetics, Yale University School of Medicine, New Haven, CT 06520. E-mail addresses: vikki.abrahams{at}yale.edu and paula.kavathas{at}yale.edu

⁶ Abbreviations used in this paper: Ct, Chlamydia trachomatis; EB, elementary body; IFU, inclusion-forming unit; MOMP, major outer membrane protein, MOI, multiplicity of infection; NI, noninfected; NLR, Nod-like receptor; RB, reticuloid body; SPG, sucrose-phosphate-glutamate.