[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address Please contact the publisher to request reinstatement.
[Skip to Content Landing]
March 1988

Mechanisms of Altered Monocyte Prostaglandin E2 Production in Severely Injured Patients

Arch Surg. 1988;123(3):293-299. doi:10.1001/archsurg.1988.01400270027003

• 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 (Ts) lymphocytes did not augment monocyte PGE2 secretion, Ts 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 Ts lymphocytes with PGE2 secretagogue activity may be responsible for elevated monocyte PGE2 production in immunosuppressed trauma patients.

(Arch Surg 1988;123:293-299)