Aims/hypothesis: The macrophage-specific glycoprotein sCD163 has emerged as a biomarker of low grade inflammation in the metabolic syndrome and related disorders. High sCD163 levels are seen in acute sepsis as result of direct lipopolysaccharide-mediated shedding of the protein from macrophage surfaces including Kupffer cells. The aims of this study were to investigate if low grade endotoxinemia in human subjects results in increasing levels of sCD163 in a cortisol-dependent manner.
Methods: We studied eight male hypopituitary patients and eight age and gender matched healthy controls during intravenous low dose LPS or placebo infusion administered continuously over 360 min. Furthermore, we studied eight healthy volunteers with bilateral femoral vein and artery catheters during a 360 minutes infusion with saline and low dose LPS in each leg respectively.
Results: Systemic low grade endotoxinemia resulted in a gradual increase in sCD163 from 1.65±0.51 mg/L (placebo) to 1.92±0.46 mg/L (LPS) at 220 min, p=0.005; and from 1.66±0.42 mg/L (placebo) to 2.19±0.56 mg/L (LPS) at 340 min, p=0.006. A very similar response was observed in hypopituitary patients: from 1.59±0.53 mg/L (placebo) to 1.83±0.45 mg/L (LPS) at 220 min, p=0.021; and from 1.52±0.53 mg/L (placebo) to 2.03±0.44 mg/L (LPS) at 340 min, p<0.001. As opposed to systemic treatment, continuous femoral artery infusion did not result in increased sCD163.
Conclusion: Systemic low grade endotoxinemia resulted in increased sCD163 to levels seen in the metabolic syndrome in both controls and hypopituitary patients. This suggests a direct and cortisol-independent effect of LPS on the shedding of sCD163. We observed no effect of local endotoxinemia on levels of serum sCD163.