Neutrophil functions in late preterm neonates with respiratory distress syndrome

INTRODUCTION The innate immune system is the first line of host defense against invading microorganisms. In order to achieve this, neutrophils must be able both to circulate freely in the blood and to migrate as adherent cells into the extravascular tissues to phagocytose and kill invading microorganisms effectively. Most studies of neutrophil function have been conducted under conditions of ambient oxygen, but inflamed sites where neutrophils operate may be extremely hypoxic. However, neutrophils need to consume oxygen to maintain the NADPH oxidasedriven respiratory burst. Previous studies that have addressed the effects of respiratory distress syndrome (RDS) on neutrophil functions suggested that neutrophil functions other than the generation of the respiratory burst are not impaired. Yet, results have been confusing and in some cases contradictory. RDS is a common problem in preterm infants which is caused primarily by deficiency of pulmonary surfactant in an immature lung. This results in significant hypoxemia and constitutes a major cause of morbidity and mortality in preterm infants. Approximately half of cases with respiratory distress syndrome are associated with infections. Our cross-sectional controlled study aimed to investigate the effect of respiratory distress syndrome in late preterm infants on different aspects of neutrophil functions.