American journal of reproductive immunology (New York, N.Y. : 1989) · 2017
A novel in vitro model of villitis of unknown etiology demonstrates altered placental hormone and cytokine profile.
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Derricott Hayley, Heazell Alexander E P, Greenwood Susan L, Jones Rebecca L
Аннотация
PROBLEM: Placental dysfunction is present over 50% of cases of stillbirth and fetal growth restriction (FGR). Villitis of unknown etiology (VUE), an inflammatory condition of the placenta characterized by maternal T cell infiltrates in the villous stroma and dysregulation of inflammatory cytokines, is more frequent in FGR and stillbirth.
METHOD OF STUDY: A novel in vitro model of placental inflammation was developed to test the hypothesis that inflammatory cells seen in VUE and/or cytokines impair placental function.
RESULTS: Coculture of placental explants with maternal leukocytes resulted in increased leukocytes in villous tissue and elevated concentrations of IL-1β, IL-1Ra, IL-6, IL-10, and IFN-γ (P≤.05). Human chorionic gonadotrophin secretion was reduced following coculture with leukocytes (P≤.01) and cytokines (P≤.05).
CONCLUSION: These observations support the hypothesis that altered placental inflammation has deleterious effects on placental function. This model could be used to further understanding about the pathophysiology of VUE and to test potential therapies.
METHOD OF STUDY: A novel in vitro model of placental inflammation was developed to test the hypothesis that inflammatory cells seen in VUE and/or cytokines impair placental function.
RESULTS: Coculture of placental explants with maternal leukocytes resulted in increased leukocytes in villous tissue and elevated concentrations of IL-1β, IL-1Ra, IL-6, IL-10, and IFN-γ (P≤.05). Human chorionic gonadotrophin secretion was reduced following coculture with leukocytes (P≤.01) and cytokines (P≤.05).
CONCLUSION: These observations support the hypothesis that altered placental inflammation has deleterious effects on placental function. This model could be used to further understanding about the pathophysiology of VUE and to test potential therapies.