The role of human decay-accelerating factor in the pathogenesis of preterm labor

Luis D. Pacheco, Gary D. Hankins, Maged M. Costantine, Garland D. Anderson, Edyta Pawelczyk, Stella Nowicki, Bogdan J. Nowicki

Research output: Contribution to journalArticlepeer-review

10 Scopus citations


Complement activation is thought to contribute to the pathogenesis of preterm labor (PTL). Decay-accelerating factor (DAF) is a natural complement pathway inhibitor. Our hypothesis was that DAF expression on maternal white blood cells (WBCs) in women with preterm labor is elevated compared with women with no preterm labor. Our secondary objective was to determine if differences in upregulation of DAF levels correlated with clinical outcomes. Serial blood samples were obtained from 30 patients with a clinical diagnosis of PTL and a control group of 30 pregnant individuals (same gestational age range) to determine DAF expression in peripheral WBCs in both groups. DAF expression was higher in women with PTL (less than 37 weeks) compared with the control group without PTL. Subjects with PTL who delivered before 34 weeks had less DAF expression and different kinetics of expression compared with those carrying pregnancies beyond 34 weeks. These data suggest that women with a clinical diagnosis of preterm labor have increased DAF expression on peripheral WBCs. Furthermore, it appears that failure to elevate DAF expression is associated with a risk of early premature delivery.

Original languageEnglish (US)
Pages (from-to)565-570
Number of pages6
JournalAmerican Journal of Perinatology
Issue number7
StatePublished - 2011


  • Preterm labor
  • complement activation
  • decay-accelerating factor

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Obstetrics and Gynecology


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