Chlamydia pneumoniae Infection in Preeclampsia

Abstract

Objective. The maternal syndrome of preeclampsia results from systemic endothelial activation by a number of factors that primarily derive from the intervillous space, so-called intervillous soup. Co-precipitants, such as innate immune activators, may lower the threshold to develop the maternal syndrome in preeclampsia. We examined whether, like atherosclerosis, preeclampsia is associated with infection with Chlamydia pneumoniae (C. pneumoniae). Study Design. A case-control study was performed on 50 women with preeclampsia, 57 women with normal pregnancies at term, and 25 non-pregnant controls. Anti-C. pneumoniae antibodies were examined by enzyme-linked immunosorbent assay and C. pneumoniae genomic DNA (gDNA) loads were measured by real-time PCR. We also performed a data synthesis of the relationship between anti-C. pneumoniae seroprevalence and preeclampsia risk. Results. Neither the number of women with measurable copy numbers of C. pneumoniae gDNA, the anti-C. pneumoniae seroprevalence, nor antibody indices of IgG, IgM, or IgA to C. pneumonia varied between groups. However, when measurable, gDNA copy numbers of C. pneumoniae were increased in women with preeclampsia compared with the normal pregnant (p < 0.05) and non-pregnant controls (p < 0.05). For women with measurable C. pneumoniae gDNA, their copy numbers were correlated with anti-C. pneumoniae IgG concentrations (r² = 0.49; p < 0.0001). Data synthesis reveals that anti-C. pneumoniae IgG seroprevalence is associated with preeclampsia risk. Conclusion. Our data suggest an association between C. pneumoniae infection and preeclampsia. While not a uniform and singular precipitant of the maternal syndrome of preeclampsia, C. pneumoniae infection may be a co-precipitant with other components of the intervillous soup. Further investigations appear warranted.

• Preeclampsia
• Chlamydia pneumoniae
• Serology
• gDNA
• Data synthesis

ACKNOWLEDGMENTS

The other members of the Toxaemia group are Mel Krajden, Keith C Choi, and Peter CK Leung, David P Speert, and Stuart Turvey. This study was funded by a New Investigator Pilot Project Grant from the Canadian Institutes of Health Research (CIHR) Institute of Infection and Immunity (to PvD). FX, LAM, SET, and PvD are the recipients of salary awards from the Michael Smith Foundation for Health Research, CIHR [FX (IWRH & STIRRHS research training programs) & PvD], and the Child and Family Research Institute (PvD).

Declaration of Interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.