BACKGROUND: The aim of this study was to investigate the role of peripheral blood mononuclear cells (PBMC) in embryo invasion at the implantation site and to estimate the effect on PBMC function of human chorionic gonadotrophin (HCG) that is secreted from the human embryo. METHODS AND RESULTS: The effect of PBMC on the invasiveness of murine embryos was examined using an invasion assay. PBMC obtained from women in early pregnancy (5-9 weeks gestation) significantly enhanced both spreading of murine embryos on Matrigel and invasion beneath the gel. These effects were greater than those of PBMC obtained from non-pregnant women in the secretory phase (cycle day 16-24) and the control (in the absence of PBMC). When PBMC obtained from non-pregnant women were incubated with recombinant HCG (10 IU/ml) for 2 days and were subjected to invasion assay using murine embryos, PBMC treated with HCG significantly promoted both spreading and invasion of murine embryos as compared with the non-treated PBMC. On the other hand, embryo outgrowth was not affected by HCG in the absence of PBMC, showing no direct effect of HCG on embryo invasion. CONCLUSION: This study indicated that PBMC from pregnant women promoted murine embryo invasion in vitro and this effect of PBMC was enhanced by HCG. These findings suggest that PBMC at the implantation site are activated by HCG secreted from the embryo, following which PBMC regulate embryo invasion.
BACKGROUND: The aim of this study was to investigate the role of peripheral blood mononuclear cells (PBMC) in embryo invasion at the implantation site and to estimate the effect on PBMC function of human chorionic gonadotrophin (HCG) that is secreted from the human embryo. METHODS AND RESULTS: The effect of PBMC on the invasiveness of murine embryos was examined using an invasion assay. PBMC obtained from women in early pregnancy (5-9 weeks gestation) significantly enhanced both spreading of murine embryos on Matrigel and invasion beneath the gel. These effects were greater than those of PBMC obtained from non-pregnant women in the secretory phase (cycle day 16-24) and the control (in the absence of PBMC). When PBMC obtained from non-pregnant women were incubated with recombinant HCG (10 IU/ml) for 2 days and were subjected to invasion assay using murine embryos, PBMC treated with HCG significantly promoted both spreading and invasion of murine embryos as compared with the non-treated PBMC. On the other hand, embryo outgrowth was not affected by HCG in the absence of PBMC, showing no direct effect of HCG on embryo invasion. CONCLUSION: This study indicated that PBMC from pregnant women promoted murine embryo invasion in vitro and this effect of PBMC was enhanced by HCG. These findings suggest that PBMC at the implantation site are activated by HCG secreted from the embryo, following which PBMC regulate embryo invasion.