Effect of ibuprofen and dexamethasone on Kupffer cell complement receptor function after endotoxemia and the phagocytosis of erythrocytes

• Published in: Circulatory shock Vol. 27; no. 3; p. 237
• Main Authors: Commins, L M, Loegering, D J, Minnear, F L
• Format: Journal Article
• Language: English
• Published: United States 01-03-1989
• Subjects: Animals; Dexamethasone - pharmacology; Dexamethasone - therapeutic use; Erythrocytes - immunology; Ibuprofen - pharmacology; Ibuprofen - therapeutic use; Immunoglobulin gamma-Chains - metabolism; Immunoglobulin gamma-Chains - pharmacology; Kupffer Cells - drug effects; Kupffer Cells - immunology; Male; Phagocytosis; Rats; Rats, Inbred Strains; Receptors, Complement - drug effects; Receptors, Complement - metabolism; Salmonella; Shock, Septic - drug therapy; Shock, Septic - immunology
• ISSN: 0092-6213

Depression of Kupffer cell complement receptor (CR) function is associated with several states of depressed host defense. This study was carried out to determine if ibuprofen and dexamethasone, which decrease the mortality rate following endotoxemia, could prevent the depression of CR function caused by endotoxemia and the phagocytosis of antibody-coated erythrocytes (EIgG). The depression of CR function caused by endotoxin was completely prevented by the administration of ibuprofen or dexamethasone. Thus, the ability of these drugs to prevent the depression of macrophage function may contribute to their salutory effects during endotoxin shock. In contrast to the effect with endotoxemia, the depression of CR function caused by the phagocytosis of EIgG was not modified by pretreatment with ibuprofen or dexamethasone. Additional studies demonstrated that the depression of CR function caused by EIgG was probably not due to EIgG in the blood or bound to Kupffer cells, interfering with the receptor probe for access to the CR. This study has shown that ibuprofen and dexamethasone can prevent the depression of CR function caused by endotoxin but not the depression caused by the phagocytosis of EIgG. These results suggest that different mechanisms mediate the depression of CR function caused by endotoxin and the phagocytosis of EIgG.