Neutrophil accumulation is a cardinal histopathological feature of acute and chronic inflammatory diseases of the gastrointestinal tract. In order for granulocytes to accumulate in an inflamed tissue, an adhesive interaction must first occur between the leukocyte and endothelial cell surface. Granulocyte adhesion begins as a rolling movement such that the leukocytes move slower than erythrocytes in the stream of blood bathing the vascular endothelium. As inflammation progresses, the number of rolling leukocytes increases and the velocity of leukocyte rolling decreases. These changes increase the probability for a strong adhesive interaction between the leukocyte and endothelial cell surface, which ultimately leads to an elevated number of stationary (adherent) leukocytes and emigration of the phagocytes into the adjacent interstitial compartment. Although the importance of these events in the overall process of inflammation has been recognized for well over a century, only recently has it become clear that leukocyte-endothelial cell adhesion is a well controlled physiological phenomenon that is influenced by both physical and chemical forces acting on cell (leukocyte and endothelium) surfaces. Physiologic factors that appear to make a significant contribution to leukocyteendothelial cell adhesion during inflammation include: 1) adhesion molecules expressed on the surface of activated neutrophils and/or endothelial cells, 2) reactive oxygen metabolites and granule-associated proteins released by activated neutrophils, and 3) hydrodynamic dispersal forces (eg, wall shear stress) that tend to sweep leukocytes away from the vascular wall. Another factor that has led to the renewed interest in modulation of leukocyte adherence is the recognition that inflammation-associated tissue injury can be ameliorated by agents which interfere with the ability of neutrophils to roll, adhere and/or emigrate in the microvasculature. Such observations suggest that drugs which act at the level of neutrophil adherence may represent a novel and effective strategy for the management of inflammatory diseases. The development and implementation of such a strategy would require a thorough understanding of the factors that govern the adhesive interactions between leukocytes and vascular endothelium.