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Release of soluble intercellular adhesion molecule 1 into bile and serum in murine endotoxin shock

Neutrophil‐induced liver injury during endotoxemia is dependent on the adhesion molecules Mac‐1 (CD11b/CD18) on neutrophils and its counterreceptor on endothelial cells and hepatocytes, intercellular adhesion molecule 1 (ICAM‐1). To investigate a potential release of a soluble form of ICAM‐1 (sICAM‐1), animals received 100 μg/kg Salmonella abortus equi endotoxin alone or in combination with 700 mg/kg galactosamine. In endotoxin‐sensitive mice (C3Heb/FeJ), injection of endotoxin did not cause liver injury but induced a time‐dependent increase of sICAM‐1 in serum (300%) and in bile (615%) without affecting bile flow. In galactosamine/endotoxin‐treated animals, which developed liver injury, the increase in both compartments was only 97% and 104%, respectively. In either case, the increase in sICAM‐1 concentrations paralleled the enhanced ICAM‐1 expression in the liver. The endotoxin‐resistant strain (C3H/HeJ) did not show elevated sICAM‐1 levels in serum or bile after endotoxin administration. In contrast, the intravenous injection of murine tumor necrosis factor α (TNF‐α), interleukin‐1α (IL‐1α) or IL‐1β (13‐23 μg/kg) into endotoxin‐resistant mice induced a 225% to 364% increase in serum sICAM‐1 and a 370% elevation of the biliary efflux of sICAM‐1, again independent of changes in bile flow. These data indicate that cytokines are major inducers of sICAM‐1 formation during endotoxemia in vivo. The described experimental model can be used to investigate the role of sICAM‐1 in the pathophysiology of inflammatory liver disease.