Dialysis-induced serum factors inhibit adherence of monocytes and granulocytes to adult human endothelial cells

Abstract

In patients on hemodialysis, the sequences of events required for adhesion molecule-mediated adherence of monocytes and granulocytes to endothelial cells are pathophysiologically disrupted because activation of the cells with subsequent alterations in adhesion molecule phenotypes takes place in the extracorporeal circuit far away from the respective endothelial cell ligand. As a consequence, the host defense to infections may be affected. We analyzed the expression of CD62L and CD11b/CD18 on monocytes and granulocytes and the adherence of these cells, collected before, during, and after cuprophan hemodialysis, to resting and interleukin-1β (IL-1β)-stimulated adult human saphenous vein endothelial cells (HSVECs). Monocytes collected before dialysis adhered more avidly to HSVECs than did granulocytes. Adherence of both cell types increased to IL-1β-stimulated HSVECs ( P < 0.05). Granulocytes obtained at 180 minutes adhered less to resting HSVECs than granulocytes harvested before hemodialysis ( P < 0.05), despite an increase in CD11b/CD 18 expression. To study if serum factors inhibiting adherence accumulate during hemodialysis, we incubated leukocytes harvested before hemodialysis in the same patients' serum collected before, during, and after dialysis. Serum collected at 180 minutes of cuprophan hemodialysis exerted inhibitory effects on both monocyte and granulocyte adhesion to HSVECs ( P < 0.05). By contrast, serum collected during polysulfone hemodialysis of the same patients did not have any significant impact on the adherence of inflammatory cells to HSVECs. These findings contribute to an increased understanding of the factors involved in the impaired immune response observed in dialysis patients.