Immune Status in Very Preterm Neonates
Azizia M et al. – These data support the concept that fetal exposure to inflammation before preterm delivery leads to subsequent endotoxin hyporesponsiveness (immunoparalysis), which increases the risk of subsequent sepsis and associated organ dysfunction.Methods
- Prospective observational study conducted at a university hospital recruiting 113 preterm neonates (23–32 weeks) and 78 controls.
- Monocyte major histocompatibility complex (MHC) class II expression, serum, and ex vivo lipopolysaccharide stimulated levels of six cytokines were measured in umbilical cord blood and over the first 7 days.
- The presence of neonatal sepsis and histologic chorioamnionitis was recorded.
- Prematurity (preterm labor and preterm premature rupture of membranes cohorts), neonatal sepsis, and histologic chorioamnionitis were associated with significant reduction in monocyte MHC class II expression.
- Neonates who had evidence of subsequent protracted sepsis had low levels of MHC class II expression at birth.
- Serial monocyte MHC class II expression revealed a fall by day 2, in all preterm neonates, with the degree being influenced by both prematurity and sepsis, and incomplete recovery by day 7, suggesting immunoparalysis in preterm premature rupture of membranes and preterm labor cohorts.
- Whole blood lipopolysaccharide stimulation assay showed significantly lower tumor necrosis factor alpha, values in preterm neonates who subsequently developed sepsis indicating a degree of immunoparalysis.