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Steve E. Calvano, PhD; Annabel E. Barber, MD; Arthur S. Hawes, MD; Herbert F. de Riesthal; Susette M. Coyle, RN; Stephen F. Lowry, MD

Arch Surg. 1992;127(2):181-186.

Abstract
• We studied the role of lipopolysaccharide and the associated hypercortisolemic response as mediators of leukocyte changes associated with endotoxemia. Normal human subjects were given continuous, 12-hour, intravenous infusions of cortisol. After 6 hours of cortisol infusion, lipopolysaccharide (20 U/kg) was administered in an intravenous bolus. Plasma cortisol and blood leukocyte counts and lymphocyte subset proportions were evaluated every hour throughout the 12-hour study period. After 6 hours of cortisol infusion, lymphocyte counts and proportions of CD4+ helper/inducer T cells had declined significantly. The fact that these cells did not decline further in response to lipopolysaccharide and continued cortisol infusion suggests that lipopolysaccharide-induced lymphocyte changes are cortisol dependent. In contrast, the granulocytosis normally observed after lipopolysaccharide administration was unaffected by cortisol infusion. Finally, the monocyte counts and proportions of B cells (HLA-DR+ or CD20+ cells) responded to cortisol infusion and LPS in a pattern distinct from that of lipopolysaccharide alone. These results indicate that lipopolysaccharide-induced hypercortisolemia plays a role in immune modulation during endotoxemia.

(Arch Surg. 1992;127:181-186)

Author Affiliations
From the Department of Surgery, Cornell University Medical College, New York, NY.

Footnotes
Accepted for publication November 2, 1991.

Presented at the 11th Annual Meeting of the Surgical Infection Society, Fort Lauderdale, Fla, April 9, 1991.

Reprint requests to the Department of Surgery, Box 177, Cornell Medical College, 525 East 68th St, New York, NY 10021 (Dr Calvano).

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