Abstract
Bacterial infection is an important cause of death and long-term morbidity in neonates, especially in immature preterm neonates. The present study clarified the defense mechanism in neonates by measuring superoxide anion (one of reactive oxygen species: ROS) production and phagocytic activity of polymorphonuclear leukocytes (PMNs) caused by live bacterial stimulation in whole blood. In neonatal PMNs, superoxide anion production was significantly diminished when stimulated with an appropriate amount of Escherichia coli (E. coli). There was no significant difference in ROS production with stimulation of Staphylococcus aureus (S. aureus) between adult and neonatal PMNs. Both adult and neonatal PMNs showed equal activity in E. coli phagocytosis. The expression of Toll-Like Receptor 2 (TLR2), Toll-Like Receptor 4 (TLR4) and CD14 on the PMNs showed no difference between neonate and adult blood. The p38 mitogen-activated protein kinase (p38 MAPK) was also activated equally with the stimulation of live bacteria in both PMNs. Since p38 MAPK is a key molecule in lipopolysaccharide binding protein (LBP)-TLR4 mediating intracellular pathway, the receptor mediated signal transduction pathways have no difference between adult and neonatal PMNs. Diminished superoxide production of neonatal PMNs with E. coli stimulation was reconstituted, when neonatal PMNs were stimulated in adult plasma. This phenomenon was abolished by the heat inactivation of adult plasma but not by the addition of anti-interferon γ or anti-tumor necrosis factor α blocking antibody. These data suggest that some heat-labile factors in whole blood might have a role in augmentation of the ROS production of neonatal PMNs, responding to E. coli.
Highlights
IntroductionEspecially in immature preterm neonates, causes death and has a key role for long-term morbidity of those infants
Bacterial infection in neonates, especially in immature preterm neonates, causes death and has a key role for long-term morbidity of those infants
We found that no significant difference in ability of superoxide production, when adult and cord blood polymorphonuclear leukocytes (PMNs) were stimulated with S. aureus
Summary
Especially in immature preterm neonates, causes death and has a key role for long-term morbidity of those infants. The reason of this phenomenon is mainly due to the immaturity of bactericidal mechanisms in innate immunity. Neutrophils (PMNs: Polymorphonuclear leukocytes) are primary responders maintaining nonspecific innate immunity against bacterial invasion [1]. The principal functions exhibited by circulating PMNs in response to bacterial invasion and inflammation include adherence to the vascular endothelium, deformability, chemotaxis, phagocytosis and intracellular microbial killing. The ability of PMNs adherence, deformability and chemotaxis are known to be low because of the immaturity of neutrophil structure [2]. Because the toxic reactive oxygen species (ROS) appear to be essential for the microbicidal activity of neutrophils [3], the possibility of a deficit in oxygen metabolism in neonatal neutrophils has been explored in several studies, but the results were controversial [4,5,6,7,8,9]
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