3,4-di-deoxyglucosone-3-ene promotes leukocyte apoptosis.

Background: Heat-sterilized, single-chambered, glucose-containing peritoneal dialysis solutions promote neutrophil apoptosis and impair the peritoneal antibacterial response. It has been proposed that glucose degradation products may be responsible for this effect. However, the precise contribution of individual glucose degradation products had not been addressed.

Regulation of apoptosis by lethal cytokines in human mesothelial cells.

Background: Dysregulation of peritoneal cell death may contribute to the complications of peritoneal dialysis (PD). Chronic peritoneal dialysis and acute peritonitis are both associated with loss of mesothelial cells. In addition, acute peritonitis is characterized by sudden changes in the number of peritoneal leukocytes.

Inhibition of caspases improves bacterial clearance in experimental peritonitis.

Background: Inhibition of caspases improves the antibacterial capacity of leukocytes cultured with peritoneal dialysis solutions, and improves the prognosis of septic, polymicrobial experimental peritonitis.

Objective: To test whether inhibition of caspases alters the evolution of peritonitis in the presence of peritoneal dialysis solution.

Design: 32 mice were assigned to therapy with either the pan-caspase inhibitor zVAD or vehicle for 48 hours following infection with Staphylococcus aureus, in the presence of lactate-buffered, 4.

Acceleration of neutrophil apoptosis by glucose-containing peritoneal dialysis solutions: role of caspases.

Commercial, glucose-containing peritoneal dialysis (PD) solutions have deleterious effects on leukocytes and mesothelial cells that contribute to an impaired peritoneal defense. However, the molecular mechanisms of these deleterious effects are poorly understood. The effect of PD solutions on neutrophil viability, the molecular mechanisms of cell death, its functional consequences, and the possibilities for pharmacologic modulation have now been studied.