Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production

A paper recently published in The Journal of Immunology describes that the effect of a Chlamydia infection on trophoblast secretion of chemokines and cytokines may have a profound impact on the microenvironment of the maternal-fetal interface and this could influence pregnancy outcome.

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.

It was 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 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, it was found that Ct infection of the trophoblast results in the cleavage and degradation of NF-KB 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 paper entitled “Chlamydia trachomatis infection modulates trophoblast cytokine/chemokine production” (Eugenia de la Torre, Melissa J. Mulla, Andrew G. Yu, Seung-Joon Lee, Paula B. Kavathas, and Vikki M. Abrahams. The Journal of Immunology, 2009, 182: 3735–3745), is the result of the research carried out by Dr. Eugenia de la Torre (researcher at the CReSA nowadays) and other collaborators in the Department of Laboratory Medicine, Immunobiology and Genetics and Department of Obstetrics, Gynecology & Reproductive Sciences, Yale University School of Medicine (New Haven).



  • To contact the author of this paper:
Dra. Maria Eugenia de la Torre Martínez
Researcher
Immunology Unit (CReSA)
Email: eugenia.torre@cresa.uab.es
Telephone no.: +34 935814565
Fax: +34 935814490
Edifici CReSA. Campus UAB
08193 Bellaterra (Barcelona) España
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