Effect of prostaglandin E1 on chemiluminescence response and adherence of human polymorphonuclear leukocytes to human cultured endothelial cells of prostaglandin E1 treated polytraumatized patients

1993 ◽  
Vol 8 (5) ◽  
pp. 253-260
Author(s):  
Eleonore Jonas ◽  
Alexander Dwenger ◽  
Michael Jonas ◽  
Michael Nerlich ◽  
Harald Tscherne
Keyword(s):  
Endothelial Cells ◽  
Polymorphonuclear Leukocytes ◽  
Prostaglandin E1 ◽  
Cultured Endothelial Cells ◽  
Human Polymorphonuclear Leukocytes

Binding and transfer of verocytotoxin by polymorphonuclear leukocytes in hemolytic uremic syndrome

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3396-3402
Author(s):  
D. Maroeska W. M. te Loo ◽  
Leo A. H. Monnens ◽  
Thea J. A. M. van der Velden ◽  
Mario A. Vermeer ◽  
Frank Preyers ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Hemolytic Uremic Syndrome ◽  
Polymorphonuclear Leukocytes ◽  
Cell Damage ◽  
Binding Studies ◽  
Single Class ◽  
Target Organs ◽  
Uremic Syndrome ◽  
Human Polymorphonuclear Leukocytes

The hemolytic uremic syndrome (HUS) is the most common cause of acute renal failure in children. The role of a verocytotoxin (VT)-producing Escherichia coli has been strongly implicated in the epidemic form of HUS. Although direct toxicity of VT on glomerular endothelial cells has been demonstrated, it remained still unclear how the VT is transported from the intestine to the target organs. In this study we demonstrate that VT, when incubated in whole blood, binds rapidly and completely to human polymorphonuclear leukocytes (PMNs) and not to other components of blood. Binding studies with125I-VT-1 showed a single class of binding sites on freshly isolated, nonstimulated human PMNs. TheKd of VT-binding to PMNs was 10-8 mol/L, 100-fold less than that of the VT-receptor globotriaosylceramide. On incubation of VT-preloaded PMNs with human glomerular microvascular endothelial cells (GMVECs), transfer of VT-1 to the endothelial cells occurred. Incubation of nonstimulated GMVECs with VT-preloaded PMNs, but not with PMNs or VT-1 alone, caused inhibition of protein synthesis and cell death. Our data are in concert with a role of PMNs in the transfer of VT from the intestine to the kidney endothelium. This transfer occurs by selective binding to a specific receptor on PMNs and subsequent passing of the ligand VT to the VT-receptor on GMVECs, which causes cell damage. This new mechanism further underpins the important role of PMNs in HUS.

Binding and transfer of verocytotoxin by polymorphonuclear leukocytes in hemolytic uremic syndrome

Blood ◽  
2000 ◽  
Vol 95 (11) ◽  
pp. 3396-3402 ◽  
Author(s):  
D. Maroeska W. M. te Loo ◽  
Leo A. H. Monnens ◽  
Thea J. A. M. van der Velden ◽  
Mario A. Vermeer ◽  
Frank Preyers ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Hemolytic Uremic Syndrome ◽  
Polymorphonuclear Leukocytes ◽  
Cell Damage ◽  
Binding Studies ◽  
Single Class ◽  
Target Organs ◽  
Uremic Syndrome ◽  
Human Polymorphonuclear Leukocytes

Abstract The hemolytic uremic syndrome (HUS) is the most common cause of acute renal failure in children. The role of a verocytotoxin (VT)-producing Escherichia coli has been strongly implicated in the epidemic form of HUS. Although direct toxicity of VT on glomerular endothelial cells has been demonstrated, it remained still unclear how the VT is transported from the intestine to the target organs. In this study we demonstrate that VT, when incubated in whole blood, binds rapidly and completely to human polymorphonuclear leukocytes (PMNs) and not to other components of blood. Binding studies with125I-VT-1 showed a single class of binding sites on freshly isolated, nonstimulated human PMNs. TheKd of VT-binding to PMNs was 10-8 mol/L, 100-fold less than that of the VT-receptor globotriaosylceramide. On incubation of VT-preloaded PMNs with human glomerular microvascular endothelial cells (GMVECs), transfer of VT-1 to the endothelial cells occurred. Incubation of nonstimulated GMVECs with VT-preloaded PMNs, but not with PMNs or VT-1 alone, caused inhibition of protein synthesis and cell death. Our data are in concert with a role of PMNs in the transfer of VT from the intestine to the kidney endothelium. This transfer occurs by selective binding to a specific receptor on PMNs and subsequent passing of the ligand VT to the VT-receptor on GMVECs, which causes cell damage. This new mechanism further underpins the important role of PMNs in HUS.

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