Abnormalities of LECAM-1- and Mac-1-Dependent Neutrophil-Endothelial Cell Adhesion in the Developing Host

Abstract

Incompletely defined inflammatory deficits contribute to infectious morbidity and mortality in human neonates and neonatal animals (1). Previous studies in neonatal animal models have demonstrated diminished or delayed emigration of blood neutrophils into extravascular inflammatory sites (2–4) which, in turn, may reflect deficits of neutrophil chemotactic functions as demonstrated by numerous in vitro investigations (5,6). To understand the molecular and functional basis for these (presumably) developmental deficits, recent studies have focused on the molecular events contributing to neutrophil-endothelial interactions in vitro and in vivo. As described in this report, significant abnormalities of CD18-dependent as well as CD18-independent adherence mechanisms appear to underlie diminished neutrophil localization and/or function (7–12). These abnormalities may contribute to impaired host defense capabilities or, alternatively, may serve a physiologic role against inflammatory injury of neonatal tissues in the postpartum setting. These possibilities will be addressed in future investigations which should exploit the neonate as a model of inflammation, to allow a further definition of its molecular basis.