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J. Jeremy Wood, BM, FRCS; John T. Grbic, DMD; Mary L. Rodrick, PhD; Andrea Jordan; John A. Mannick, MD

Arch Surg. 1987;122(2):179-184.

Abstract
• We performed studies using an animal model of thermal injury to confirm the observed decrease in interleukin 2 (IL-2) production in burned patients and to explore the underlying mechanisms. Ten mice subjected to a 25% scald were compared with ten anesthetized littermates (controls) and six untreated mice (normal mice) 1,3, 5,7,10,14, and 21 days after burn. Production of IL-2 by splenocytes was stimulated by concanavalin A alone, or in the presence of the cyclooxygenase inhibitor indomethacin or flurbiprofen. The IL-2 content of the resulting supernatant was determined by the response of the IL-2-dependent cell line CTLL-2. The IL-2 production was significantly suppressed in the burned mice at three days (mean ± SEM, 30.9% ± 5.2%), five days (19% ± 5.5%), seven days (41.6%±6.4%), and 21 days (20%±4.5%). Significant enhancement of IL-2 production by indomethacin was seen in the burned group (mean, 95%), but not in controls (mean, 23.8%) or normal mice (mean, 17.2%), and similar effects were seen with flurbiprofen. In separate experiments the effects of exogenous prostaglandin E₂ on lymphocyte blastogenesis and IL-2 production were studied, and an increased susceptibility to the inhibitory effects of prostaglandin E₂ was observed following thermal injury.

(Arch Surg 1987;122:179-184)

Author Affiliations
From the Department of Surgery, Brigham & Women's Hospital/Harvard Medical School, Boston. Dr Wood is now with Whipps Cross Hospital, London.

Footnotes
Accepted for publication Oct 6, 1986.

Read before the Sixth Annual Meeting of the Surgical Infection Society, Chicago, April 21, 1986.

Reprint requests to Brigham and Women's Hospital, 75 Francis St, Boston, MA 02115 (Dr Mannick).

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