Amniotic Membrane is an Immunosuppressor of Peripheral Blood Mononuclear Cells

Abstract

Amniotic membrane (AM) is the inner layer of the placenta, which is in contact with the fetus; it has been used for transplantation in ocular surface diseases. It has been reported that amniotic membrane promotes epithelialization, inhibits angiogenesis and diminishes ocular inflammation. A persistent epithelial defect is the delay in epithelial wound healing caused by infiltrating inflammatory cells into the cornea and amniotic membrane transplantation has been successfully used in its treatment, however the mechanism of action in inhibiting inflammation it is not well understood. This study was aimed at determining whether denuded amniotic membrane (dAM) induces anti-inflammatory effects on peripheral blood mononuclear cells. Methods: Human peripheral blood mononuclear cells (PBMC) were cultured on dAM. Proliferation and apoptosis assays were performed on PBMC; and synthesis and secretion of pro-inflammatory cytokines by these cells was analyzed. Results: dAM induced apoptosis and inhibited cell proliferation of PBMC; and abolished the synthesis and the secretion of pro-inflammatory cytokines even when they were LPS stimulated. In contrast, when PBMC were cultured on hydrophilic membrane cell culture inserts, apoptosis was not significantly induced, cell proliferation was conserved, and synthesis and secretion of pro-inflammatory cytokines were not affected. Conclusions: Taken together, these results could explain the anti-inflammatory in vivo effects observed when the amniotic membrane is used as a transplant.

Keywords:

• Amniotic membrane
• Immunosuppressor
• Proinflammatory cytokines

ACKNOWLEDGMENTS

This work was partially financed by grants from CONACyT SALUD-096-01; INPer 212250-06131; and Conde de Valenciana Foundation. The authors wish to thank Guadalupe Quintero, Jessica Nieves, Mariana Garcia and Veronica Romero for their technical support.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.