The purpose of this review is to summarize the current knowledge of the biochemical activities and the potential cellular source(s) of the inflammatory marker procalcitonin (PCT). PCT has been proven to be a reliable indicator for the diagnosis of sepsis. Since serum-PCT concentrations correlate with the severity of the disease, routine PCT measurements became of prognostic value for the monitoring of septic patients. This correlation supports the concept that PCT exhibits detrimental effects within the host organism (e.g. via contribution to the deleterious fall in blood pressure observed in the advanced state of sepsis). However, no precise information is available to date concerning PCTs mode of action and its cellular origin during the inflammatory process. In recent studies, we could show that PCT affects the generation of nitric oxide (NO) and tumor necrosis factor-α (TNF). Both NO and TNF-α are markedly elevated in the plasma of septic patients and it is suggested that they play a role as mediators or modulators for the onset of septic shock. It is imminent to further investigate the role of PCT within the inflammatory cascade, its effects on other inflammatory agonists as well as to gain further insight into the signal transduction mechanisms following cellular activation by PCT. The characterization of PCT with respect to its origin and its biochemical functions will provide further insight into the pathogenesis of sepsis and septic shock, and detailed knowledge of PCTs mode of action are an essential prerequisite for potential therapeutical interventions directed towards PCT metabolism.
Keywords: nitric oxide, procalcitonin, sepsis, systemic inflammation, tumor necrosis
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