Effect of anti-PGE antibody on cell-mediated immune response in thermally injured mice.
Prostaglandin E (PGE) production is elevated in burn-injured individuals and has been implicated as a mechanism in thermal injury-induced immunosuppression. Profound depression of cell-mediated immune response (CMIR) is a characteristic effect of burn injury, and was evaluated using the popliteal lymph node assay for graft-versus-host and host-versus-graft responsiveness in mice. Preservation of CMIR after burn injury was observed in animals treated with 40 mg/kg ibuprofen and in mice given anti-PGE antibody. It appears that PGE is a central immunoregulatory mediator of suppressed CMIR following thermal injury and that treatment resulting in inhibition of PGE production or neutralization of PGE with anti-PGE antibody prevented burn-induced immunosuppression.
Freeman
T R
TR
Department of Surgery, University of Utah Medical Center, Salt Lake City.
Shelby
J
J
D000818:Animals; D000906:Antibodies / Q000627:therapeutic use*; D002056:Burns / Q000276:immunology*; D006087:Graft vs Host Reaction; D006789:Host vs Graft Reaction; D007052:Ibuprofen / Q000627:therapeutic use; D007111:Immunity, Cellular; D007165:Immunosuppression Therapy; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D011458:Prostaglandins E / Q000037:antagonists & inhibitors / Q000276:immunology*
D000906:Antibodies; D011458:Prostaglandins E; D007052:Ibuprofen