Abstract
Pre-eclampsia (PE) is thought to be a pregnancy-induced autoimmune disease. Despite several strategies carried out for targeting specific factors relevant to its pathogenesis, PE remains potentially fatal to some patients. Here, we reported a way to isolate mesenchymal stem cells (MSCs) from decidua. The MSCs not only exhibited differentiation and self-renewal capacities, they also possessed immunomodulatory functions and secreted some soluble mediators including IL-6, TGF-β, IDO, VEGF and COX-2. Most importantly, the MSCs were specifically provided with the ability to suppress T cells proliferation by IDO in response to inflammatory cytokine IFN-γ. Moreover, we developed a Th1 cell-induced PE mouse model which displayed a high level of pathogenesis factor TNF-α. Strikingly, MSCs-based therapy significantly ameliorated both clinical and histopathological severity of PE symptoms including decreasing the blood pressure and proteinuria, suppressing glomerulonephritis, protecting the feto-placental development. The therapy also reversed abnormal TNF-α expression in uterine and splenic lymphocytes. These data suggest that MSCs may ameliorate Th1-induced PE-like symptoms in mice via the suppression of TNF-α and MSCs-based therapy may provide a potential novel method for PE.
Highlights
PE is a common obstetric syndrome affecting women in their first pregnancy and characterized by hypertension and proteinuria which appeared after 20 weeks of gestation
There is a shift of cytokine production toward Th2-type immunity with predominance of IL-4 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) [4], pregnancy is considered as a Th2 phenomenon
A novel way was developed for isolating mesenchymal stem cells (MSCs) from human decidua here.In general, an enzyme cocktail instead of collagenase was used here to digest the fragments of decidua
Summary
PE is a common obstetric syndrome affecting women in their first pregnancy and characterized by hypertension and proteinuria which appeared after 20 weeks of gestation. There is a shift of cytokine production toward Th2-type immunity with predominance of IL-4 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) [4], pregnancy is considered as a Th2 phenomenon. In PBMC derived from some women with PE, Th1 cytokines expression increased and Th2 cytokines expression decreased, implying the balance shifts toward Th1-type immunity[5,6,7]. It was reported that TNF-a was involved in the activation of autoantibody-mediated angiotensin receptor. Both TNF-a and angiotensin receptor autoantibody affected the production of soluble fms-like tyrosine-1 and soluble endoglin, which are two critical etiological factor in PE [13,14]. TNF-a has been speculated to contribute to pathogenesis of this disease
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