title: Increased concentrations of cytokines interleukin-6 and interleukin-1 receptor antagonist in plasma of women with preeclampsia: a mechanism for endothelial dysfunction?
abstract: OBJECTIVE
  To determine if plasma concentrations of defined cytokines are increased in women with preeclampsia, and to correlate any increases with the elevated concentrations of the vascular cell adhesion molecule (VCAM)-1.
  
  
  METHODS
  Twenty primigravidas with preeclampsia were compared to 20 healthy primigravidas. Plasma levels of cytokines, tumor necrosis factor-alpha (TNF alpha), interleukin (IL)-6, IL-8, IL-1 beta, IL-1 receptor antagonist (IL-1ra), granulocyte macrophage-colony-stimulating factor (GM-CSF), and VCAM-1, were measured by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Concentrations of IL-6 and IL-1ra were significantly higher (P < .01) in preeclamptic women (2.56 and 251.85 pg/mL, respectively) compared to normal pregnant patients (2.06 and 142.00 pg/mL, respectively). There were no significant changes in concentrations of TNF alpha, IL-8, GM-CSF, and IL-1 beta in preeclamptic patients (14.09, 50.52, 125.8, and 2.08 pg/mL, respectively) compared to normal patients (11.96 44.46, 121.3, and 2.01 pg/mL, respectively). Serum concentrations of VCAM-1 were increased in women with preeclampsia (preeclamptic group 841.9 +/- 49.7 ng/mL, control group 560.2 +/- 47.9 ng/mL; t = 3.673, P < .001). Interleukin-6 and IL-1ra concentrations correlated with VCAM-1 concentrations (IL-6: r = 0.539, z = 2.9, P < .005; IL-1ra: r = 0.451, z = 2.428, P < .02).
  
  
  CONCLUSIONS
  Increased cytokine concentrations may contribute to the endothelial damage that occurs with preeclampsia and may explain the mechanism underlying leukocyte activation in this disorder. The increased cytokine concentration may also be responsible for the endothelial adhesion that accompanies preeclampsia.
authors.affiliation: Department of Obstetrics and Gynecology, Royal Infirmary, Glasgow, Scotland, United Kingdom.
authors.forename: I A
authors.initials: IA
authors.lastname: Greer
authors.forename: F
authors.initials: F
authors.lastname: Lyall
authors.forename: T
authors.initials: T
authors.lastname: Perera
authors.forename: F
authors.initials: F
authors.lastname: Boswell
authors.forename: L M
authors.initials: LM
authors.lastname: Macara
mesh_terms: D000328:Adult; D015815:Cell Adhesion Molecules / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000097:blood; D006801:Humans; D007375:Interleukin-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood*; D016209:Interleukin-8 / Q000097:blood; D011225:Pre-Eclampsia / Q000097:blood* / Q000503:physiopathology; D011247:Pregnancy; D017472:Receptors, Interleukin-1 / Q000037:antagonists & inhibitors*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: D015815:Cell Adhesion Molecules; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D017472:Receptors, Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D016178:Granulocyte-Macrophage Colony-Stimulating Factor