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Decreased superoxide production, degranulation, tumor necrosis factor alpha secretion, and CD11b/CD18 receptor
D Kaufman1, L Kilpatrick, R G Hudson
1Division of Neonatology, Department of Pediatrics, University of Pennsylvania School of Medicine, The Children's Hospital of Philadelphia, Joseph Stokes Jr. Research Institute, Philadelphia, Pennsylvania 19104-4399, USA. dak4r@virginia.edu
Insights
Preterm infants exhibit weakened immune responses due to deficient monocyte adherence and function. This impacts their ability to fight infections, highlighting potential targets for therapeutic intervention.
Area of Science:
- Neonatal immunology
- Infectious disease in neonates
Background:
- Preterm infants have higher infection rates due to immature immune systems.
- Monocyte adherence is crucial for immune cell localization and antimicrobial activity.
Purpose of the Study:
- To investigate monocyte adhesion and immune functions in preterm infants.
- To compare these functions with those of full-term infants.
Main Methods:
- Isolation of cord blood monocytes from preterm and full-term infants.
- Assessment of monocyte adherence, superoxide generation, degranulation, cytokine secretion (TNF-α, IL-1β, IL-6), and adhesion receptor expression (CD11b/CD18).
Main Results:
- Adherent monocytes from preterm infants showed significantly reduced superoxide production (28%) and degranulation (37%).
- Tumor necrosis factor alpha secretion was decreased by 35% in stimulated adherent monocytes from preterm infants.
- Significantly lower expression of CD11b/CD18 adhesion receptors was observed in monocytes from preterm infants (60% and 52% decrease).
Conclusions:
- Monocyte adherence and associated immune functions are impaired in preterm infants.
- Reduced expression of CD11b/CD18 receptors may contribute to diminished monocyte adherence and immune response.
- Monocyte adherence factors could be key in modulating immune responses in preterm neonates.
Abstract:
Preterm infants have an increased incidence of infection, which is principally due to deficiencies in neonatal host defense mechanisms. Monocyte adherence is important in localizing cells at sites of infection and is associated with enhanced antimicrobial functions. We isolated cord blood monocytes from preterm and full-term infants to study their adhesion and immune functions, including superoxide (O2-) generation, degranulation, and cytokine secretion and their adhesion receptors. O2- production and degranulation were significantly diminished, by 28 and 37%, respectively, in adherent monocytes from preterm infants compared to full-term infants (P < 0. 05); however, these differences were not seen in freshly isolated cells. We also observed a significant decrease of 35% in tumor necrosis factor alpha secretion by lipopolysaccharide-stimulated adherent monocytes from preterm infants compared to full-term infants (P < 0.05); however, this difference was not observed in interleukin-1beta or interleukin-6 production by the monocytes. The cell surface expression of the CD11b/CD18 adhesion receptor subunits was significantly decreased (by 60 and 52%, respectively) in monocytes from preterm infants compared to full-term infants (P < 0. 01). The cascade of the immune response to infection involves monocyte upregulation and adherence via CD11b/CD18 receptors followed by cell activation and the release of cytokines and bactericidal products. We speculate that monocyte adherence factors may be important in the modulation of immune responses in preterm infants.