Prostaglandin E2 (PGE2)-dependent suppression of interleukin alpha (IL-2) production in patients with major trauma.

摘要: The depression of interleukin-2 synthesis represents a major dysfunction within the cascade immunologic defects induced by mechanical and thermal trauma. This study was undertaken to elucidate negative control mechanisms that were responsible for deficiency IL-2 production in polytraumatized patients. Peripheral blood mononuclear cells (PBMC's) from 29 patients (average age, 35.8 years; average ISS, 35) separated on post-trauma days 1, 3, 5, 7, 10, 14, 21 cultured as untreated (C), treated with indomethacin (C + INDO), depleted adherent (C-AC). Cell cultures assayed proliferative responses PHA, synthesis, PGE2 production, gamma-interferon levels, phenotyping studies. On all there found marked reduction compared controls highly significant nadir day 5 10 an almost 80% inhibition (p less than 0.005). C INDO showed increases over ranging 48% (Day 1) 220% 7). Removal (C-AC) did not reverse suppression production. levels depressed parallel but increase INDO. PBMC's OKT3+, OKT4+, IL-2R+ lymphocytes well elevation monocyte 0.005) count. There monocytes, due monocytosis higher capacity individual following peaked Day 7 at 400% These data suggest post trauma is caused mainly two factors: excessive output inhibitory monocytes inadequate function immature and/or blocked lymphocytes. partial restoration suggests blockade cyclo-oxygenase pathway immunomodulating therapy may some abnormalities multiple