title: Fetuses delivered following preterm prelabor rupture of the membranes are capable of stimulating a proinflammatory response in endothelial cells.
abstract: OBJECTIVE
  Preterm premature rupture of the membranes (PROM) has been attributed to ascending infection and a choriodecidual inflammatory response (ie, on the maternal side). However, on the fetal side those most at risk of morbidity have a systemic proinflammatory cytokine response. We have recently defined a similar proinflammatory response in pregnancies complicated by vascular disease on the fetal side of the placenta. A factor(s) present in fetal plasma from these pregnancies can stimulate human umbilical vein endothelial cells (HUVECs) to express mRNA for the proinflammatory cytokines, interleukin (IL)-6 and IL-8. The hypothesis of this study was that a similar factor(s) was present in preterm PROM.
  
  
  METHODS
  A standard culture of HUVECs was incubated with fetal plasma, obtained immediately following delivery, from normal pregnancies delivering vaginally at term (n=16) and pregnancies delivering following preterm PROM (n=19). Expression of mRNA for IL-6 and IL-8 was assessed by reverse transcription polymerase chain reaction (RT-PCR) and standardized to GAPDH mRNA expression.
  
  
  RESULTS
  Endothelial cell expression of IL-6 mRNA (median [25-75th centile] 0.295 [0.252-0.507] vs term vaginal delivery 0.208 [0.151-0.307]; P=.009) was enhanced in response to the fetal plasma from PROM cases compared to pregnancies delivering vaginally at term. In contrast, mRNA expression of IL-8 (median [25-75th centile] preterm PROM 0.41 [0.21-0.78] vs term vaginal delivery 0.49 [0.16-0.68]; P=.46) was not different in the two groups.
  
  
  CONCLUSIONS
  We have demonstrated that in fetuses delivered following preterm PROM there is a factor(s) capable of stimulating a local endothelial cell proinflammatory cytokine (IL-6) response. This factor(s) that we have demonstrated may be responsible for the increased cytokine production seen in fetuses with the fetal inflammatory response syndrome.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Sydney/Westmead Hospital, Westmead NSW, Australia.
authors.forename: Neil
authors.initials: N
authors.lastname: Athayde
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Xin
authors.initials: X
authors.lastname: Wang
authors.forename: Brian
authors.initials: B
authors.lastname: Trudinger
mesh_terms: D004730:Endothelium, Vascular / Q000276:immunology*; D005260:Female; D005322:Premature Rupture of Fetal Membranes / Q000276:immunology*; D006801:Humans; D007231:Infant, Newborn; D015850:Interleukin-6 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics / Q000276:immunology*; D016209:Interleukin-8 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics / Q000276:immunology*; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D015850:Interleukin-6; D016209:Interleukin-8; D012333:RNA, Messenger