PROBLEM: The objective of this study was to clarify the role of the main proinflammatory cytokines (interleukin [IL]-1, IL-6, tumor necrosis factor [TNF]-alpha) in the pathogenesis of preeclampsia and how these cytokines affect one another and the production of prostaglandins (PGs). METHOD OF STUDY: The concentrations of cytokines and PGs in supernatants of placental tissue from preeclamptic and normal women were determined by enzyme-linked immunosorbent assay. RESULTS: The concentrations of the PGs from unstimulated preeclamptic placental tissue were significantly higher compared to the concentrations of PGs from normal unstimulated placental tissue. Significant levels of IL-1beta were observed only in the supernatants of preeclamptic placental tissue. Of interest, an increase in TNF-alpha production was detected in the supernatants of IL-1-stimulated preeclamptic placental tissue. CONCLUSIONS: The overproduction of TNF-alpha may be related not only to the effect of a stimulant like IL-1beta, but mainly to the lack of mechanisms down-regulating the production of TNF-alpha.
PROBLEM: The objective of this study was to clarify the role of the main proinflammatory cytokines (interleukin [IL]-1, IL-6, tumornecrosis factor [TNF]-alpha) in the pathogenesis of preeclampsia and how these cytokines affect one another and the production of prostaglandins (PGs). METHOD OF STUDY: The concentrations of cytokines and PGs in supernatants of placental tissue from preeclamptic and normal women were determined by enzyme-linked immunosorbent assay. RESULTS: The concentrations of the PGs from unstimulated preeclamptic placental tissue were significantly higher compared to the concentrations of PGs from normal unstimulated placental tissue. Significant levels of IL-1beta were observed only in the supernatants of preeclamptic placental tissue. Of interest, an increase in TNF-alpha production was detected in the supernatants of IL-1-stimulated preeclamptic placental tissue. CONCLUSIONS: The overproduction of TNF-alpha may be related not only to the effect of a stimulant like IL-1beta, but mainly to the lack of mechanisms down-regulating the production of TNF-alpha.
Authors: G S Stødle; G B Silva; L H Tangerås; L M Gierman; I Nervik; U E Dahlberg; C Sun; M H Aune; L C V Thomsen; L Bjørge; A-C Iversen Journal: Clin Exp Immunol Date: 2018-04-23 Impact factor: 4.330
Authors: Melissa J Mulla; Jane E Salmon; Larry W Chamley; Jan J Brosens; Crina M Boeras; Paula B Kavathas; Vikki M Abrahams Journal: PLoS One Date: 2013-06-06 Impact factor: 3.240