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Interleukin 2 Primes and Activates Kupffer Cells to Suppress Hepatocyte Protein Synthesis In Vitro

Ronald D. Curran, MD; Timothy R. Billiar, MD; Michael A. West, MD; Brandon G. Bentz; Richard L. Simmons, MD

Arch Surg. 1988;123(11):1373-1378.

Abstract
• Interleukin 2 (IL-2) is an essential mediator of the immune response and has also been shown to be protective in experimental models of sepsis. Macrophages have IL-2 receptors but their function is unknown. We investigated the effect of IL-2 on Kupffer cells, the fixed macrophages of the liver, using an in vitro rat hepatocyte—Kupffer cell coculture system. In this model, endotoxin (lipopolysaccharide) triggers Kupffer cells to induce suppression of hepatocyte protein synthesis. We found that pretreatment with 10 U/mL or more of IL-2 primed Kupffer cells, significantly reducing the concentration of lipopolysaccharide necessary to trigger Kupffer cell—mediated suppression of hepatocyte protein synthesis. Higher concentrations of IL-2 (1 x10⁴ U/mL) alone were capable of priming and triggering Kupffer cells to suppress hepatocyte protein synthesis. These data show that IL-2 increases Kupffer cell sensitivity to endotoxin, suggesting that IL-2 may play an important role in regulating macrophage responses to septic stimuli.

(Arch Surg 1988;123:1373-1378)

Author Affiliations
From the Departments of Surgery, University of Pittsburgh (Drs Curran, Billiar, and Simmons and Mr Bentz) and University of Minnesota, Minneapolis (Dr West).

Footnotes
Accepted for publication June 21, 1988.

Read before the Eighth Annual Meeting of the Surgical Infection Society, San Francisco, May 5, 1988.

Reprints not available.

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