The microcirculation and inflammation: modulation of leukocyte-endothelial cell adhesion

TLDR

Leukocyte accumulation in inflamed tissue arises from adhesive interactions between leukocytes and endothelial cells in postcapillary venules, governed by adhesion molecule expression, reactive oxygen/nitric oxide products, and blood flow shear forces. The study examines how different adhesion molecules mediate leukocyte rolling, adherence, and emigration, explores endogenous anti‑adhesion molecules and shear‑rate effects, and evaluates the pathophysiological implications for adhesion‑targeted therapies in cardiovascular and circulatory disorders. J Leukoc Biol 55:662–675 (1994).

Abstract

Abstract The accumulation of leukocytes in inflamed tissue results from adhesive interactions between leukocytes and endothelial cells within the microcirculation. These adhesive interactions and the excessive filtration of fluid and protein that accompanies an inflammatory response are largely confined to one region of the microvasculature: postcapillary venules. The nature and magnitude of the leukocyte–endothelial cell adhesive interactions that take place within postcapillary venules are determined by a variety of factors, including expression of adhesion molecules on leukocytes and/or endothelial cells, products of leukocyte (superoxide) and endothelial cell (nitric oxide) activation, and the physical forces generated by the movement of blood along the vessel wall. The contribution of different adhesion molecules to leukocyte rolling, adherence, and emigration in venules is discussed. Emerging views on potential endogenous antiadhesion molecules produced by endothelial cells as well as the influence of alterations in shear rate on leukocyte adhesion are addressed. Finally, the pathophysiological significance of the microvascular responses to inflammation are discussed in terms of adhesion-directed strategies for the treatment of different cardiovascular diseases and circulatory disorders. J. Leukoc. Biol. 55: 662–675; 1994.