Sepsis is one of the leading morbidity and mortality factors in newborns, occurring in more than 700 of every 100000 live births. 1 Newborns seem to have a unique susceptibility to early bacterial infections2 compared with adults, but the underlying pathomechanisms are still poorly defined. Neutrophils represent the first and most powerful cellular line of antibacterial host defense, as they are able to kill most bacteria within a few hours. 3 These innate immune cells engulf and destroy pathogens intracellularly, a phenomenon known for more than 100 years as phagocytosis. 4 In 2004, Brinkmann et al described for the first time a mechanism of how neutrophils kill bacteria extracellularly: neutrophil extracellular trap (NET) formation or NETosis. 5, 6 Upon stimulation, neutrophils undergo cytoplasmic and nuclear changes, the intracellular architecture is lost, and chromatin fibers are expelled that contain DNA, histones, and granular proteins to form NETs, a machinery used to trap and destroy bacteria surrounding the dying neutrophil. 7

Recently, Yost and coworkers reported that neonatal neutrophils are impaired in NET formation, which may explain why newborns are prone to bacterial infections. 8 Here, we present experimental data that complement and extend these findings and add to our understanding of how NETosis is regulated in newborns. Yost et al stimulated neonatal (cord blood–derived) and adult neutrophils for 1 hour with lipopolysaccharide (LPS) or platelet-activating factor