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Gary A. Keller, MD; Michael A. West, MD; John T. Harty; Frank B. Cerra, MD; Richard L. Simmons, MD

Arch Surg. 1985;120(2):180-186.

Abstract
• The etiology of hepatic failure associated with the multiple-system organ failure syndrome is poorly understood. Because of indirect evidence suggesting that macrophages or Kupffer's cells may play a role in this phenomenon, macrophage-rich peritoneal cells were co-cultured with isolated rat hepatocytes. Following co-culture, the rate of hepatocyte protein synthesis, quantitated by counts per minute of tritiated leucine incorporated into protein, was significantly diminished. This modulation of hepatocyte function was not enhanced by prestimulation of macrophage-rich peritoneal cells in vivo by casein, thioglycolate, or Corynebacterium parvum. Addition of the macrophage secretory product lysozyme did not alter hepatocyte protein synthesis. This cell-mediated effect on hepatocytes could not be recreated by a macrophage-rich peritoneal cells supernatant transfer. These results support the idea that cells of macrophage lineage could mediate changes in hepatocyte function that may, in turn, play a role in the etiology of hepatic malfunction associated with the multiple-system organ failure syndrome.

(Arch Surg 1985;120:180-186)

Author Affiliations
From the Division of Surgical Infectious Diseases, Department of Surgery, University of Minnesota, Minneapolis.

Footnotes
Accepted for publication Aug 10, 1984.

Read before the Fourth Annual Meeting of the Surgical Infection Society, Montreal, May 1, 1984.

Reprints not available.

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