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J Surg Res. 1998 Apr;76(1):27-31.

Endotoxemia and IL-1 beta stimulate mucosal IL-6 production in different parts of the gastrointestinal tract.

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Department of Surgery, University of Cincinnati, Ohio, USA.



In recent studies, sepsis and endotoxemia were associated with increased IL-6 production in mucosa of the jejunum. We tested the hypothesis that endotoxemia in mice stimulates mucosal IL-6 production in other parts of the gastrointestinal tract as well and that the enterocyte is a source of mucosal IL-6. In addition, we examined the effects of TNF alpha and IL-1 beta on mucosal IL-6 production.


Endotoxin (12.5 mg/kg) was injected subcutaneously in mice. Control mice were injected with a corresponding volume of sterile saline. After 4 h, IL-6 levels were determined in mucosa of stomach, jejunum, ileum, and colon and in plasma and liver. In a second series of experiments, immunohistochemistry was performed of jejunal mucosa to determine in which cell type IL-6 was expressed. Finally, 100 micrograms/kg of human recombinant TNF alpha or human recombinant IL-1 beta was injected intraperitoneally in mice and IL-6 levels were determined in plasma and tissues after 4 h.


Endotoxemia resulted in increased mucosal IL-6 levels in small and large bowel but in reduced IL-6 levels in gastric mucosa. Immunohistochemistry of jejunal mucosa showed that IL-6 was expressed mainly in the enterocyte and in a few cells of the lamina propria. Treatment of mice with TNF alpha reduced IL-6 levels in gastric mucosa whereas IL-1 beta increased IL-6 levels in mucosa of small intestine.


Mucosal IL-6 production during endotoxemia is differentially regulated along the gastrointestinal tract. Both TNF alpha and IL-1 beta may be involved in the regulation of gastrointestinal IL-6 production during endotoxemia.

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