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24: Trophoblast infection with chlamydia pneumoniae induces placental dysfunction and preeclampsia

      Objective

      Chlamydia pneumoniae has been associated with atherosclerotic vascular disease. In pregnancy, placental vascular disease results from failed trophoblast invasion and may cause adverse reproductive outcomes, including preeclampsia. We sought to determine if C. pneumoniae infection impairs extravillous (invasive) trophoblast cell function and is associated with preeclampsia.

      Study Design

      We conducted cell viability and invasion assays using primary extravillous trophoblast cells isolated from first trimester placentas. Cells were infected for 24-48 hours with C. pneumoniae (0.1-1.0 inclusion forming units/cell). In order to correlate C. pneumoniae infection of the placenta with obstetrical outcomes, we performed a case-control study to identify C. pneumoniae DNA by PCR in trophoblast cells dissected by laser-capture microscopy from placentas in 48 women with severe preeclampsia (cases) and 30 women who delivered at term without any obstetrical or medical complications (controls).

      Results

      The viability of extravillous trophoblast cells was decreased significantly after infection with C. pneumoniae, P<0.05. Extravillous trophoblast cell invasion through an extracellular matrix also was decreased after infection with C. pneumoniae; invasion rates were normalized to 1.0 in non-infected cells, and invasion rates were reduced to 0.6-0.8 after infection with C. pneumoniae, P<0.05. In our case-control study, C. pneumoniae DNA was detected in placental trophoblast cells in 15/48 cases (31%) and 3/30 controls (10%), OR=0.41, P=0.02, Fisher exact test. Positive and negative PCR controls yielded expected results.

      Conclusion

      Chlamydia pneumoniae can infect human placental trophoblast cells and reduce trophoblast invasion into the uterine wall. Women with preeclampsia have higher rates of C. pneumoniae detection in the placenta than controls. Further investigation of the mechanisms by which C. pneumoniae induces trophoblast dysfunction, and the identification of novel therapeutic strategies to prevent adverse outcomes attributed to trophoblast dysfunction, are warranted.