Prolactin modifies the in vitro LPS-induced chemotactic capabilities in human fetal membranes at the term of gestation.

Abstract

ProblemImmune responses of fetal membranes involve the production of chemoattractant mediators causing infiltration of maternal and fetal leukocytes, intrauterine inflammation and potentially the disruption of maternal‐fetal tolerance. Prolactin (PRL) has deep immunoregulatory effects in the fetal‐maternal interface. We aimed to test the in vitro PRL effect upon chemotactic capacities of human fetal membranes.Method of StudyFetal membranes and umbilical cord blood were collected from healthy non‐laboring caesarean deliveries at term. Fetal membranes were cultured in Transwell® frames to mimic the barrier function between choriodecidual and amniotic sides. Tissues were treated with PRL, Lipopolysaccharide (LPS), or both simultaneously. Then, RANTES, MCP‐1, MIP‐1α, IP‐10, and PECAM‐1 were quantified in a conditioned medium by choriodecidual or amniotic sides. The chemotaxis of subsets of migrating mononuclear cells from umbilical cord blood was evaluated in a Boyden Chamber in response to the conditioned medium by both sides.ResultsLipopolysaccharide stimulates the production of RANTES, MCP‐1, MIP‐1α, and PECAM‐1 in choriodecidua, while MIP‐1α and PECAM‐1 only increase in amnion. PRL decrease RANTES, MCP‐1, and MIP‐1 only in choriodecidua, but PECAM‐1 was decreased mainly in amnion. The leukocyte migration was regulated significantly in response to the conditioned medium by the amnion, increase in the conditioned medium after LPS treatment, contrary with, the leukocyte migration decreased in a significant manner in response to conditioned medium after PRL and LPS‐PRL co‐treatment. Finally, T cells were the most responsive subset of cells.ConclusionsProlactin modified in a tissue‐specific manner the chemotactic factor and the leukocyte migration differentially in fetal membranes.