摘要：CD14 is membrane-associating or free soluble glycoprotein which recognizes lipopolysaccharide (LPS) and is assumed to be involved in the onset of endotoxin shock. There are some reports suggesting the relationship between increased expression of CD14 in infectious or inflammatory diseases. However, little has been reported concerning the soluble CD14 (sCD14) level, especially in mice. In this study, we measured the plasma level of sCD14, TNF-α and IL-6 in the iota-carrageenan (CAR)-primed endotoxin shock model in addition to the D -galactosamine ( D -galN)-primed endotoxin shock model mice. It was confirmed that all mice were dead within 12 h after a higher dose of LPS-treatment in both animal models. The level of TNF-α, IL-6 and sCD14 significantly increased in the CAR-primed endotoxin shock model mice. However, the D -galN-primed endotoxin shock model mice showed only a slight increment of TNF-α and IL-6 level, and sCD14 was below the detectable level. In the examination using several doses of LPS in CAR-primed model mice, IL-6 and sCD14 were increased dependent on the LPS dose, but TNF-α remained at an almost equal level at any dose of LPS in this study condition. In conclusion, the production of TNF-α, IL-6 and sCD14 was significantly enhanced in the CAR-primed model mice, compared to the D -galN-primed model mice. Therefore, these data indicate the possibility that the sCD14 level did not increase consistently, even under a fatal condition in endotoxin shock. Also, CAR-primed endotoxin shock would be an important experimental model to examine the elevation mechanisms for sCD14 and IL-6 production.
关键词：CD14;lipopolysaccharide;endotoxin shock model mice;tumor necrosis factor (TNF)-α;interleukin (IL)-6
