title: PP127. CMV infection and TLR2 expression in HELLP syndrome.
abstract: BACKGROUND
  The HELLP syndrome is a serious complication in pregnancy characterized by haemolysis, elevated liver enzymes and low platelet count occurring in 10-20% of cases with severe preeclampsia and associated with metabolic disorders symptoms later in life. Emerging evidence indicated that cytomegalovirus (CMV) infection and TLR signaling activation are associated with severe preeclampsia and metabolic disorder conditions.
  
  
  OBJECTIVE
  The aim of this study was to examine CMV sero-prevalence and its associated TLR signaling activation in patients with HELLPs.
  
  
  METHODS
  A case-control study was performed. Subjects included women with HELLP syndrome (n=6) and normal pregnancy controls (n=20), who matched with cases for maternal age, gestational age and parity. Maternal serum CMV serology and cytokines response were measured by ELISA. TLR2 and TLR4 expression on peripheral Neutrophils were detected by real-time PCR.
  
  
  RESULTS
  CMV IgG seropositivity was more prevalent among HELLP syndrome patients than normal pregnancy controls (85% versus 40%, p<0.01). Patients with HELLP syndrome also had elevated TLR2 (p<0.01) and IL-1β mRNA expressions (p<0.05) and increased TNF-α: IL-10 (p<0.05) and IL-6: IL-10 (p<0.05) ratio compared with matched normal pregnancy controls.
  
  
  CONCLUSIONS
  It is important to consider pregnancy CMV infection through TLR2 signaling in modulation of innate immune response in maternal HELLP syndrome, and may be linked with increased metabolic disorders later in life.
authors.affiliation: Institute for Systems Biology, Seattle, United States.
authors.forename: F
authors.initials: F
authors.lastname: Xie
authors.affiliation: Child and Family Research Institute, Vancouver, Canada.
authors.forename: Y
authors.initials: Y
authors.lastname: Hu
authors.affiliation: Child and Family Research Institute, Vancouver, Canada.
authors.forename: P
authors.initials: P
authors.lastname: von Dadelszen
authors.affiliation: Institute for Systems Biology, Seattle, United States.
authors.forename: J
authors.initials: J
authors.lastname: Nadeau