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March 1988

Alteration of Monocyte Function Following Major Injury

Author Affiliations

From the Departments of Surgery (Drs Faist, Mewes, Ertel, and Heberer) and Medicine (Dr Strasser), Klinikum Grosshadern, Ludwig-Maximilians University, Munich; Theodor Kocher Institute, University of Bern, Bern, Switzerland (Dr Walz); Department of Immunology, Ciba-Geigy Ltd Research Center, Basel, Switzerland (Dr Alkan); and Department of Surgery, Yale University School of Medicine, New Haven, Conn (Dr Baker).

Arch Surg. 1988;123(3):287-292. doi:10.1001/archsurg.1988.01400270021002

• The macrophage exerts its stimulatory and regulatory functions within the specific immune response via the interleukin 1 (IL-1) and prostaglandin E2 (PGE2), respectively. In a screening study of macrophage-related variables following injury, a total of 58 patients (mean age, 32 years; mean Injury Severity Score, 38), macrophagic phenotyping with the monoclonal antibody Leu M3 and serial measuring of the antagonistic monokines IL-1 and PGE2 and of the macrophage-activating lymphokine interferon gamma were carried out on posttrauma days 0,1,3,5,7,10,14, and 21. The posttraumatic course was characterized by significant monocytosis, showing a peak value of 32% of Leu M3—positive cells compared with 15% of these cells in normal control subjects. During the posttrauma course, the macrophagic PGE2 output was significantly elevated up to eightfold on days 5 and 7 compared with that of control subjects (0.441 ±0.14 ng/mL vs 0.052 ± 0.01 ng/mL). Conversely, macrophagic IL-1 synthesis was significantly suppressed until day 10. Levels of interferon gamma were suppressed to a significant degree during the two-day observation period, with a trend to slow recovery at the end of week 3. These data suggest that a negative regulatory macrophagic function may be the event initiating posttraumatic immunosuppression. To restore impaired macrophagic T-helper cell interaction, cyclo-oxygenase inhibition and substitution of interferon gamma may be useful to potentiate facilitatory macrophagic function and to block inhibitory macrophagic activity.

(Arch Surg 1988;123:287-292)