Macrophage Activation Decreases Macrophage Prostaglandin E2 Release in Experimental Trauma

作者：Henry A. Pretus, I. William Browder, PETER LUCORE, Rose B. McNamee, Ernest L. Jones, David Lee Williams · 发表于：The Journal of Trauma: Injury, Infection, and Critical Care · 年份：1989 · DOI：10.1097/00005373-198908000-00014 · 被引用次数：19 · 研究领域：Immune Response and Inflammation、Wound Healing and Treatments、Surgical site infection prevention

Prostaglandin E2 (PGE2) derived from macrophages following trauma may contribute to trauma-induced immunosuppression. This study evaluated the effect of glucan, a macrophage-activating agent, on macrophage PGE2 release in a murine trauma model. ICR/HSD mice were administered D5W, glucan pre-trauma, or glucan post-trauma, and subjected to hindlimb crush and amputation injury. Splenic macrophages were isolated 24 hours following trauma, cultured (24 hrs), and macrophage PGE2 levels were determined. In-vitro marrow proliferation was assessed as a measure of immune function. Crush-amputation injury increased (184%) macrophage PGE2 release. In contrast, glucan administration (pre or post) reduced PGE2 levels in macrophage supernatants (71% and 85%, respectively). A 52% decrease in in-vitro bone marrow proliferation was observed following trauma. Glucan pre- or post-trauma eliminated the suppression of bone marrow proliferation. In conclusion, macrophage-activating immunomodulators may exert beneficial effects following trauma by: 1) reducing macrophage PGE2 synthesis and release; and 2) reducing traumatic suppression of bone marrow proliferation.