Selective immuno-modulatory effect of prolactin upon pro-inflammatory response in human fetal membranes

• Published in: Journal of reproductive immunology 2017-09, Vol.123, p.58-64
• Main Authors: Flores-Espinosa, Pilar, Preciado-Martínez, Eduardo, Mejía-Salvador, Araceli, Sedano-González, Gabriela, Bermejo-Martínez, Luisa, Parra-Covarruvias, Adalberto, Estrada-Gutiérrez, Guadalupe, Vega-Sánchez, Rodrigo, Méndez, Isabel, Quesada-Reyna, Braulio, Olmos-Ortiz, Andrea, Zaga-Clavellina, Veronica
• Format: Article
• Language: English
• Subjects: Amnion - immunology; Anti-Inflammatory Agents - metabolism; Cells, Cultured; Chorioamniotic membranes; Choriodecidual inflammation; Decidua - immunology; Female; Humans; Immunomodulation; Inflammation Mediators - metabolism; Interleukin-10 - metabolism; Lipopolysaccharides - immunology; Maternal-fetal interface; Neuroimmunomodulation; Organ Culture Techniques; Placental Circulation; Pregnancy; Prolactin; Prolactin - metabolism
• ISSN: 0165-0378; 1872-7603
• DOI: 10.1016/j.jri.2017.09.004

•Prolactin exert a differential immune-modulatory effect on human fetal membranes.•Prolactin inhibits human choriodecidual membrane inflammation.•Prolactin plays a key role in the maintenance of amniotic cavity as an immune-privileged site.•Prolactin decrease the secretion of IL-1β and TNFα in a significant fashion.•Prolactin can induce an important increase of IL-10 secretion in human fetal membranes. During pregnancy, prolactin (PRL) is a neuro-immuno-cytokine that contributes actively to the crosstalk between the immune and endocrine systems and, thus, to the creation of an immune-privileged milieu. This work aims to analyze the capacity of PRL to modulate the synthesis and secretion of pro-inflammatory markers associated with labor. Studies were conducted using human fetal membranes at term mounted in a model of two independent chambers. The choriodecidual region was stimulated with 500-ng/mL lipopolysaccharide (LPS), and the amnion and choriodecidual region were co-simulated with different concentrations of PRL that can arise during pregnancy: 250, 500, 1000, and 4000ng/mL. Following these co-treatments, the tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10 levels were measured in both compartments. As expected, treatment with LPS induced all cytokines to increase. Co-stimulation with the highest tested concentration of PRL induced significant decreases in TNF-α in the choriodecidual region and IL-1β in both regions of the fetal membranes. PRL did not modified the IL-6 and IL-10 secretion profile. These findings, coupled with clinical evidence, suggest that the high level of PRL in the amniotic cavity is involved the mechanism by which the fetal-placental unit regulates the equilibrium between pro- and anti-inflammatory modulators.