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.
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Abbreviations
- CS:
-
cesarean section
- LPS:
-
lipopolysaccharide
- TLR-4:
-
toll-like receptor-4
- VD:
-
vaginal delivery
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We thank all of the parents and staff who consented to donate blood samples to this project.
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Supported by grants from the Health Research Board of Ireland (Clinical Research Fellowship to E.J.M.); the Mater College, Ireland; and the Children' Research Fund, Our Lady's Hospital for Sick Children, Ireland.
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Molloy, E., O'Neill, A., Grantham, J. et al. Labor Promotes Neonatal Neutrophil Survival and Lipopolysaccharide Responsiveness. Pediatr Res 56, 99–103 (2004). https://doi.org/10.1203/01.PDR.0000130473.30874.B6
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DOI: https://doi.org/10.1203/01.PDR.0000130473.30874.B6
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