Delays in leukocyte localization likely contribute to diminished host defense in neonates. Understanding the processes which may be affected has been hampered by lack of suitable developmental models. Using intravital microscopy we examine directly leukocyte recruitment in a rabbit pup model. In response to intraperitoneal IL-1ß, there were three fold fewer leukocytes that arrested in pup mesenteric vessels and emigrated compared to adult, though leukocyte flux was not different. Leukocyte rolling velocity in pups was one half that in adult. In response to surgical trauma alone, the number of arrested pup cells was 15% that of adult, though again leukocyte flux was not different. An anti-L-selectin antibody inhibited rolling significantly by 60 min for both pups and adults. The effect on arrest and emigration occurred at significantly earlier times, though was less in rabbit pups. A primary defect in leukocyte emigration in the rabbit pup appears to be a failure of the cell to transition efficiently from rolling to arrest. L-selectin-dependent adhesion and emigration is decreased, rolling is not, suggesting that at least part of the defect is due to events downstream of the initial tether.