|Smith, C Wayne|
Submitted to: American Journal of Physiology - Heart and Circulatory Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/26/2001
Publication Date: 2/1/2002
Citation: Mariscalco, M.M., Vergara, W., Mei, J., Smith, O.E., Smith, W.C. 2002. Mechanisms of decreased leukocyte localization in the developing host. American Journal of Physiology - Heart and Circulatory Physiology. 282(2):H636-644. Interpretive Summary: This study investigates neonatal defense mechanisms for fighting infection using a rabbit pup model. Functional abnormalities related to leukocyte mobility are shown to be unrelated to recruitment from the blood stream, but rather related to a decreased ability to transition from rolling to arrest.
Technical Abstract: Delays in leukocyte localization likely contribute to diminished host defense in neonates. Understanding the processes that may be affected has been hampered by the lack of suitable developmental models. Using intravital microscopy, we directly examine leukocyte recruitment in a rabbit pup model. In response to intraperitoneal interleukin (IL)-1beta, there were one-third as many leukocytes that arrested in pup mesenteric vessels and emigrated compared with adult vessels, although leukocyte flux was not different. Leukocyte rolling velocity in pups was one-half that in adults. In response to surgical trauma alone, the number of arrested pup cells was 15% that of adult cells, although 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, although the effect 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 are decreased, rolling is not, suggesting that at least part of the defect is due to events downstream of the initial tether.