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November 1994

Systemic and Liver Cytokine ActivationImplications for Liver Regeneration and Posthepatectomy Endotoxemia and Sepsis

Author Affiliations

From the Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY.

Arch Surg. 1994;129(11):1159-1164. doi:10.1001/archsurg.1994.01420350057006

Background:  The liver is known to be an important site of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) production during infection, but local changes in these cytokines after liver resection are unknown.

Design:  Fischer rats were subjected to 70% hepatectomy or sham operation to determine if hepatic resection alters liver cytokine production and subsequent response to infection.

Results:  During liver regeneration, circulating IL-6 levels were mildly increased but no expression of TNF-α or IL-6 could be detected in the regenerating livers. However, the capacity for the regenerating liver to produce cytokines was intact, since intraperitoneal Escherichia coli endotoxin (2 mg/kg) produced liver cytokine messenger RNA levels in hepatectomized animals comparable to those in pair-fed controls. Systemic response to endotoxin and sepsis was also intact after hepatectomy, as circulating cytokine response was similar between hepatectomized and pair-fed animals after endotoxin administration as well as after cecal ligation and puncture.

Conclusion:  Hepatectomy elicits a circulating cytokine response without effects on liver IL-6 or TNF-α production. However, cytokine defense mechanisms are intact during noncomplicated liver regeneration, as indicated by normal TNF-α and IL-6 responses to endotoxemia or sepsis. Endotoxemia is a more potent stimulus for liver cytokine production than local trauma or liver regeneration, suggesting that not only the proximity to injury but also the severity and mechanisms of injury determine local cytokine responses.(Arch Surg. 1994;129:1159-1164)