Decreased superoxide production, degranulation, tumor necrosis factor alpha secretion, and CD11b/CD18 receptor expression by adherent monocytes from preterm infants

Preterm infants have an increased incidence of infection, which is principa lly due to deficiencies in neonatal host defense mechanisms. Monocyte adher ence is important in localizing cells at sites of infection and is associat ed with enhanced antimicrobial functions. We isolated cord blood monocytes from preterm and full-term infants to study their adhesion and immune funct ions, including superoxide (O-2(-)) generation, degranulation, and cytokine secretion and their adhesion receptors, O-2(-) production and degranulatio n were significantly diminished, by 28 and 37%, respectively, in adherent m onocytes from preterm infants compared to full-term infants (P < 0.05); how ever, these differences were not seen in freshly isolated cells. We also ob served a significant decrease of 35% in tumor necrosis factor alpha secreti on by lipopolysaccharide-stimulated adherent monocytes from preterm infants compared to full-term infants (P < 0.05); however, this difference was not observed in interleukin-1 beta or interleukin-6 production by the monocyte s. The cell surface expression of the CD11b/CD18 adhesion receptor subunits was significantly decreased (by 60 and 52%, respectively) in monocytes fro m preterm infants compared to full-term infants (P < 0.01). The cascade of the immune response to infection involves monocyte upregulation and adheren ce via CD11b/CD18 receptors followed by cell activation and the release of cytokines and bactericidal products. We speculate that monocyte adherence f actors may be important in the modulation of immune responses in preterm in fants.