title: Placental blood leukocytes are functional and phenotypically different than peripheral leukocytes during human labor.
abstract: Rupture of the fetal membranes during human labor is associated with an inflammatory process localized to the maternal-fetal interface. There is evidence that specific leukocytes subsets are attracted to the choriodecidua, and that after homing they condition a local inflammatory microenvironment, possibly being directly involved in rupture of the membranes. In this study our aim was to compare the phenotypes and function of leukocytes located in the placental intervillous blood with peripheral leukocytes obtained before or after labor, including expression of modulators of inflammation in these cells. Flow cytometry revealed that the proportion of CD14(+) cells is increased in intervillous blood, suggesting the participation of monocytes/macrophages during labor. Real time qRT-PCR showed that at term gestation and particularly during labor, placental blood leukocytes adopt a different expression pattern of pro-inflammatory cytokines than leukocytes in peripheral blood, including IL-1beta and IL-1RA. During labor, both placental and peripheral leukocytes increase their secretion of matrix metalloproteinase-9. Moreover, we showed that placental leukocytes respond differently than peripheral leukocytes to bacterial lipopolysaccharide, secreting differential amounts of TNF-alpha, IL-1beta and IL-6. Finally, a preliminary proteomic characterization of placental leukocytes revealed a significantly higher number of individual proteins than in peripheral leukocytes. Our results support the existence of selective subsets of leukocytes recruited to the maternal-fetal interface that may participate in the triggering of parturition.
authors.affiliation: Research Direction, Instituto Nacional de Perinatologia Isidro Espinosa de los Reyes, Mexico City, Mexico.
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Vega-Sanchez
authors.forename: Nardhy
authors.initials: N
authors.lastname: Gomez-Lopez
authors.forename: Arturo
authors.initials: A
authors.lastname: Flores-Pliego
authors.forename: Susana
authors.initials: S
authors.lastname: Clemente-Galvan
authors.forename: Guadalupe
authors.initials: G
authors.lastname: Estrada-Gutierrez
authors.forename: Alejandro
authors.initials: A
authors.lastname: Zentella-Dehesa
authors.forename: Rolando
authors.initials: R
authors.lastname: Maida-Claros
authors.forename: Jorge
authors.initials: J
authors.lastname: Beltran-Montoya
authors.forename: Felipe
authors.initials: F
authors.lastname: Vadillo-Ortega
mesh_terms: D005321:Extraembryonic Membranes / Q000276:immunology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology; D053590:Interleukin 1 Receptor Antagonist Protein / Q000276:immunology; D053583:Interleukin-1beta / Q000276:immunology; D015850:Interleukin-6 / Q000276:immunology; D007743:Labor, Obstetric / Q000276:immunology*; D007962:Leukocytes / Q000276:immunology*; D018950:Lipopolysaccharide Receptors / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D020780:Matrix Metalloproteinase 9 / Q000276:immunology; D009000:Monocytes / Q000276:immunology; D010920:Placenta / Q000276:immunology*; D011135:Polysaccharides, Bacterial / Q000276:immunology; D011247:Pregnancy; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D011135:Polysaccharides, Bacterial; D014409:Tumor Necrosis Factor-alpha; D020780:Matrix Metalloproteinase 9