Diapedesis of leukocytes under inflammatory conditions

At inflammatory sites or at sites of vascular injury, the adhesiveness of endothelial cells for leukocytes is increased and results in enhancement of the number of leukocytes traversing the endothelium and an invasion of the extravascular, inflamed, tissues. Both processes are regulated by the local generation and secretion of inflammatory mediators, which in turn regulate the expression of adhesion molecules on the surface of the cells involved. This can be mimicked by treatment of leukocytes or cultured endothelium, in vitro, with cytokines, such as IL-la, tumor necrosis factor a or interferon y, or with chemoat-tractants such as anaphylatoxin C5a, leukotriene B4, formylmethionyl peptides (e.g. fMLP) or chemokines (e.g. IL-8 or MCP-1). These studies revealed that expression of the various adhesion molecules on endothelial cells is often transient and depends on the type of stimulus. This is well illustrated in endothelial cells treated with the proinflammatory cytokine IL-1. Within a few minutes of activation these endothelial cells express high levels of P-selectin, which returns to basal levels within an hour; several hours after activation, surface expression of E-sel-ectin is maximal, returning to basal levels within 1 day; about a day after activation, ICAM-1 and VCAM-1 expression reach relatively stable plateau levels. These changes in surface expression of endothelial adhesion molecules most likely correlates with the shift from granulocyte to monocyte and lymphocyte extravasation that is observed in vivo about 6-24 hours after the onset of inflammation.

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