Lymphocyte binding to and penetration through vascular endothelium is stimulated by platelet-activating factor.

Lymphocytes have an important role in acute inflammatory reactions such as acute allograft rejection. Recirculating lymphocytes attach to vascular endothelium and penetrate through it into tissue parenchyma. Many recent studies have shown that different protein mediators, like gamma interferon, interleukin 1, and tumour necrosis factor enhance lymphocyte binding to and penetration through the endothelium, i.e. lymphocyte homing. We investigated the effect of platelet-activating factor (PAF) in lymphocyte binding and penetration in vitro. Treatment of rat heart microvascular endothelial monolayers with PAF (10(-6)-10(-10) M) increased the lymphocyte binding up to 1.6-fold. The effect is dose- and time-dependent. The PAF effect was reversible upon removal of the agonist: 60 min after removal of PAF no increase in the lymphocyte binding was detected. Pretreatment of endothelial cells, lymphocytes, or both of these cell types led to an increase in lymphocyte binding to endothelial monolayers. The effect of PAF in lymphocyte penetration through endothelium was investigated by using endothelial cell monolayers cultured on top of millipore filters. An optimal PAF dose (10(-8) M) for 10 min increased the number of lymphocytes penetrating through the endothelial cell monolayer into the filter by a factor of 3. These results suggest that PAF has no important role in lymphocyte homing, since it can activate the endothelial cells, the lymphocytes, or both cell types.