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Open Access Research article

Procalcitonin neutralizes bacterial LPS and reduces LPS-induced cytokine release in human peripheral blood mononuclear cells

Giovanni Matera1*, Angela Quirino1, Aida Giancotti1, Maria Concetta Pulicari1, Linda Rametti1, Maria Luz Rodríguez2, Maria Carla Liberto1 and Alfredo Focà1

Author Affiliations

1 Institute of Microbiology, Department of Medical Sciences, University “Magna Graecia” of Catanzaro, I-88100, Catanzaro, Italy

2 Randox Laboratories Limited, 5 Diamond Rd., Crumlin, County Antrim, BT29, 4QY, United Kingdom

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BMC Microbiology 2012, 12:68  doi:10.1186/1471-2180-12-68

Published: 8 May 2012

Abstract

Background

Procalcitonin (PCT) is a polypeptide with several cationic aminoacids in its chemical structure and it is a well known marker of sepsis. It is now emerging that PCT might exhibit some anti-inflammatory effects. The present study, based on the evaluation of the in vitro interaction between PCT and bacterial lipopolisaccharide (LPS), reports new data supporting the interesting and potentially useful anti-inflammatory activity of PCT.

Results

PCT significantly decreased (p < 0.05) the limulus amoebocyte lysate (LAL) assay reactivity of LPS from both Salmonella typhimurium (rough chemotype) and Escherichia coli (smooth chemotype). Subsequently, the in vitro effects of PCT on LPS-induced cytokine release were studied in human peripheral blood mononuclear cells (PBMC). When LPS was pre-incubated for 30 minutes with different concentrations of PCT, the release of interleukin-10 (IL-10) and tumor necrosis factor alpha (TNFα) by PBMC decreased in a concentration-dependent manner after 24 hours for IL-10 and 4 hours for TNFα. The release of monocyte chemotactic protein-1 (MCP-1) exhibited a drastic reduction at 4 hours for all the PCT concentrations assessed, whereas such decrease was concentration-dependent after 24 hours.

Conclusions

This study provides the first evidence of the capability of PCT to directly neutralize bacterial LPS, thus leading to a reduction of its major inflammatory mediators.