When a bacterial infection occurs, toll-like receptors flag the presence of microbial toxins. Inflammatory cytokines, such as Interleukin 1 beta (IL-1ß), Tumor Necrosis Factor alpha (TNF-α) and Interleukin 6 (IL6), are simultaneously secreted from the cell. Signaling pathways then stimulate PCT transcription, typically over three to six hours.8, 9
If the pathogen is not contained, infection spreads and the body up-regulates pro-inflammatory mediators, causing a dramatic increase in serum PCT for another 12 to 24 hours.10
It can take nearly 24 hours of appropriate antibiotic therapy to see reduction in plasma PCT levels as the bacterial infection is controlled, which will be reflected in a decrease in PCT production and circulating concentrationsby up to 50% per day. However, if initial antibiotic therapy or source control is not adequate, bacteria will continue to stimulate PCT production and blood concentrations will remain high.11
During viral infections, PCT production is lessened by Interferon gamma (IFN-γ) that is released during the host response to the virus.11 Thus, PCT concentration will not rise in viral infections as it does in the presence of a bacterial infection.
The utility of PCT as a tool for assessing the risk of bacterial infection stems from its unique kinetics, triggered from the inflammatory response to a bacterial infection.