Abstract
The tumor necrosis factor-alpha (TNF-α) cytokine receptor system modulates apoptosis in many cell types, so we have investigated the role of sTNFR1 in bacterial lipopolysaccharide (LPS)-induced cell death in cultured human decidual stromal cells, hypothesizing that sTNFR1 might play a central role in this action. In this work we characterized in vitro decidual stromal cell viability with LPS treatment and LPS and sTNFR1 co-treatment. We found that LPS treatment induced decidual stromal cell death in a dose-dependent manner and that sTNFR1 blocked the effect of the LPS treatment. There was a significant proliferation among cells co-incubated with LPS at 10 μg/mL and sTNFR1 at 0.1 μg/mL compared with LPS and sTNFR1 at 0.01, 0.05, 0.2 and 0.5 μg/mL (p < 0.01). This study demonstrated that LPS led to decidual stromal cell death in vitro but sTNFR1 down-regulates the cell death due to LPS under the same conditions. Taken together, these results suggested that sTNFR1 could participate in a protective mechanism against endotoxin.
Highlights
The immune system is tightly regulated during pregnancy in order to avoid rejection of the semiallogenic fetus, and this seems to contribute to the development of a normal pregnancy
The mean ± SEM spectrophotographic optical density for the cultured decidual stromal cell (DSC) when exposed to various concentrations of LPS was 0.42 ± 0.03, 0.39 ± 0.01, 0.30 ± 0.02, 0.37 ± 0.01, 0.36 ± 0.02 at 10 ng/mL, 100 ng/mL, 10 μg/mL, 100 μg/mL, and 1 mg/mL of LPS, respectively
The results described in this study show that TNFR1 expression at the mRNA and protein level is present in unstimulated DSCs, in accordance with observations reported by Arntzen and Menon [19,20]
Summary
The immune system is tightly regulated during pregnancy in order to avoid rejection of the semiallogenic fetus, and this seems to contribute to the development of a normal pregnancy. Cytokines are believed to be important in maintaining pregnancy and in the initiation of labor in humans. Tumor necrosis factor-alpha (TNF-α) is a multifunctional Th1 cytokine with roles in regulating hormone synthesis, placental architecture, and embryonic development [1]. Increased placental TNF-α levels have been associated with pregnancy failure in mice [2], and elevated serum TNF-α levels are associated with the first-trimester threatened abortion-complicated pregnancies with adverse outcome in humans [3]. It is believed that TNF-α promotes apoptotic cell death in fetal membrane tissues [6] and prolonged or excessive production of TNF-α represents an important etiologic factor in inflammatory-based tissue injury [7]
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