Oxidative burst and phagocytosis of neonatal neutrophils confronting Candida albicans and Candida parapsilosis.
Academic Article
Overview
abstract
BACKGROUND: Candida albicans and Candida parapsilosis are important causes of sepsis among premature neonates. The neutrophil is a key element in the control of Candida infections, yet specific neutrophil mechanisms that may contribute to the susceptibility of the premature neonate to candidiasis are not well understood. AIMS: The hypothesis for this study is that neonatal neutrophils have a developmental deficiency in their capacity to generate an oxidative burst in response to Candida species. STUDY DESIGN: Neutrophils were isolated from cord blood of term and preterm infants and from peripheral blood of adult volunteers. Neutrophils were exposed to Candida species, and assays of oxidative burst and phagocytosis were conducted. RESULTS: Oxidative burst of neutrophils from term and preterm (22-29 weeks) neonates exposed to C. albicans hyphae was similar to adult neutrophils. No detectable burst was induced in either group by exposure to C. parapsilosis yeast, and was attenuated by exposure to C. albicans yeast. Because no deficiency in oxidative burst was seen, phagocytosis was also studied. Phagocytosis of unopsonized C. albicans yeast was low in both adult and neonatal neutrophils (10-12%), but was more efficient with C. parapsilosis as target (76-88%). Neutrophils from both term and preterm infants were capable of phagocytosis equivalent to adults. CONCLUSION: A deficiency in generation of an oxidative burst or phagocytosis may not contribute to the increased susceptibility of preterm neonates to infections with Candida.
