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Carol L. Miller-Graziano, PhD; Mitchell Fink, MD; Jia Yan Wu, PhD; Gyongyi Szabo, MD; Karen Kodys

Arch Surg. 1988;123(3):293-299.

Abstract
• Monocytes from immunosuppressed trauma (11 patients) and burn (12 patients) patients stimulated with muramyl dipeptide, a potent prostaglandin E₂ (PGE₂) secretagogue, showed twofold greater PGE₂ production compared with normal controls or immunocompetent patients. Monocyte plasminogen activator production was markedly depressed and inversely correlated to patients' monocyte hyper PGE₂ production. Levels of the PGE₂-producing monocyte subset (selected as high-affinity Fc+ receptors) were progressively elevated after injury in immunosuppressed patients, reaching 65% to 80% of the total monocyte population (39% for normal controls). Although early T-suppressor (T_s) lymphocytes did not augment monocyte PGE₂ secretion, T_s lymphocytes that appeared late (>12 days after injury), during chronic infection, acted as monocyte PGE₂ secretagogues. Posttraumatic increases in monocyte sensitivity to PGE₂ secretagogues augmented the numbers of PGE₂-secreting monocytes, and the appearance of T_s lymphocytes with PGE₂ secretagogue activity may be responsible for elevated monocyte PGE₂ production in immunosuppressed trauma patients.

(Arch Surg 1988;123:293-299)

Author Affiliations
From the Departments of Molecular Genetics and Microbiology (Drs Miller-Graziano, Wu, and Szabo) and Surgery (Drs Miller-Graziano, Fink, Wu, and Szabo and Ms Kodys), University of Massachusetts Medical Center, Worcester.

Footnotes
Accepted for publication July 16, 1987.

Read before the Seventh Annual Meeting of the Surgical Infection Society, Philadelphia, May 11, 1987.

Reprint requests to Department of Surgery, University of Massachusetts Medical Center, 55 Lake Ave N, Worcester, MA 01655 (Dr Miller-Graziano).

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