Cytokine, chemokines and integrin levels in the severely preterm placenta distinguish between preeclampsia and other preinatal complications

• Published in: American journal of reproductive immunology (1989) 2006-06, Vol.55 (6), p.400-401
• Main Authors: McElrath, T F, Allred, EN, Hecht, J L, Fichorova, R N, Leviton, A
• Format: Article
• Language: English
• ISSN: 1046-7408; 1600-0897
• DOI: 10.1111/j.1600-0897.2006.00383_24.x

Using a multiplex protein array, we tested the hypothesis that the concentrations of inflammatory proteins within placental chorionic stroma differ by perinatal complication. The chorionic plates of 30 singleton placentas were biopsied immediately after delivery for severe preeclampsia (PE), membrane rupture (pPROM) or preterm labor (PL) between 23-28 weeks and flash frozen after the amnion was removed. After thawing and homogenization, concentrations of select proteins were measured on the MesoScale Discovery platform. Analytes were grouped by the functional categories of: inflammation (IL1 beta , IL6, TNF alpha , IL18,), chemotaxis (IL8), endothelial effectors (P- and E-selectin, VCAM1, ICAM1, ICAM3, VEGF) and inflammatory modulation (IL10, TGF beta , IL1ra, thrombomodulin). ANOVA and K-means clustering examined differences between delivery indications. K-means clustering distinguished PE placentas from the others, but did not discriminate PL from pPROM. Both PL and pPROM had distinct subsets of placentas with either increased inflammatory or increased modulatory activity. PE placentas tended to have low concentrations of one inflammation indicator (IL-18 P = 0.04), two endothelial effectors (E-selectin P = 0.02; ICAM1 P = 0.03), and one inflammation modulator (IL1ra P = 0.01). On the other hand, PE placentas also had elevated levels of 2 inflammation modulators (TGF beta P = 0.04; thrombomodulin P < 0.001) and elevated levels of one endothelial effector (VEGF P < 0.001). The placental inflammatory response differs by perinatal complication. The PE response has limited inflammatory activation and elevated VEGF levels. The PL and pPROM placentas appeared similar in their distribution of subgroups with inflammatory or modulatory responses. This suggests possible common pathologic antecedents and progression.