title: Labor promotes neonatal neutrophil survival and lipopolysaccharide responsiveness.
abstract: Labor is a mild proinflammatory state that is associated with fetal leukocytosis. Elective cesarean section has been linked with increased neonatal morbidity, which may be partially immune mediated. We hypothesized that labor may alter neutrophil phenotype and thereby decrease neonatal complications. We characterized neutrophil function and survival in normal neonates after either uncomplicated vaginal delivery (VD) or elective cesarean section (CS) without labor. Spontaneous neutrophil apoptosis is delayed in cord blood neutrophils of neonates after normal labor (VD) compared with CS, as assessed by propidium iodide DNA incorporation using flow cytometry. This demonstrates their ability to maintain an inflammatory response. CD11b expression on neonatal neutrophils after CS is decreased, providing further evidence of altered activation or priming. Lipopolysaccharide responsiveness, characterized by CD11b and apoptosis, is similar in VD and adults, but CS-derived neutrophils are unresponsive. Baseline TLR-4 levels are elevated in CS in contrast to the other groups, although expression is not up-regulated by lipopolysaccharide co-incubation. Neonatal neutrophil survival and function are altered by labor and may increase antibacterial function and neutrophilia. This suggests that labor of any duration may be immunologically beneficial to the normal term neonate.
authors.affiliation: Department of Surgery, Mater Misericordiae University Hospital, University College Dublin, Dublin, Ireland.
authors.forename: Eleanor J
authors.initials: EJ
authors.lastname: Molloy
authors.forename: Amanda J
authors.initials: AJ
authors.lastname: O'Neill
authors.forename: Julie J
authors.initials: JJ
authors.lastname: Grantham
authors.forename: Margaret
authors.initials: M
authors.lastname: Sheridan-Pereira
authors.forename: John M
authors.initials: JM
authors.lastname: Fitzpatrick
authors.forename: David W
authors.initials: DW
authors.lastname: Webb
authors.forename: R William G
authors.initials: RW
authors.lastname: Watson
mesh_terms: D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D002470:Cell Survival / Q000187:drug effects / Q000276:immunology; D002585:Cesarean Section; D036861:Delivery, Obstetric; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007231:Infant, Newborn; D007743:Labor, Obstetric / Q000276:immunology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008562:Membrane Glycoproteins / Q000378:metabolism; D009504:Neutrophils / Q000166:cytology* / Q000276:immunology* / Q000378:metabolism; D010641:Phenotype; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000276:immunology; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors; D014621:Vagina
chemical_list: D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D011956:Receptors, Cell Surface; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D051193:Toll-Like Receptors