Tumor necrosis factor-alpha gene expression and release in cultured human dermal microvascular endothelial cells.

Endothelial dysfunctions in the microcirculation are a common finding in the course of inflammatory disorders. These are, at least in part, mediated by endogenous agonists, e.g.

Procalcitonin amplifies inducible nitric oxide synthase gene expression and nitric oxide production in vascular smooth muscle cells.

Objective: Elevated procalcitonin concentrations are found in the course of systemic inflammation caused by bacterial insults, for example, sepsis and septic shock. However, the source of procalcitonin and its role in the inflammatory process are still unknown. In clinical studies, procalcitonin concentrations reflected the severity of sepsis and were predictive of mortality, suggesting that an increased procalcitonin synthesis is detrimental for the host.