ArticleBMC microbiology2012
Procalcitonin neutralizes bacterial LPS and reduces LPS-induced cytokine release in human peripheral blood mononuclear cells.
Article in BMC microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 37 citations in OpenAlex.
- CAR-T cell therapy-related cytokine release syndrome and therapeutic response is modulated by the gut microbiome in hematologic malignancies.Nature communications · 2022Trial
- High procalcitonin in Gram-negative urosepsis: indicator of immune modulation rather than poor outcome.World journal of urology · 2026Article
- The Role of Gut Microbiota in the Clinical Outcome of Septic Patients: State of the Art and Future Perspectives.International journal of molecular sciences · 2023Review
- Inactivation of the gene encoding procalcitonin prevents antibody-mediated arthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Relationship between calcium dynamics and inflammatory status in the transition period of dairy cows.JDS communications · 2023Review
- Predictive role of selected biomarkers in differentiating gram-positive from gram-negative sepsis in surgical patients: a retrospective study.Anaesthesiology intensive therapy · 2023Article
- Risk Factors for Elevated Serum Lipopolysaccharide in Acute Dengue and Association with Clinical Disease Severity.Tropical medicine and infectious disease · 2020Article
- Ex vivo modelling of the formation of inflammatory platelet-leucocyte aggregates and their adhesion on endothelial cells, an early event in sepsis.Clinical and experimental medicine · 2019Article
- Removal of Procalcitonin and Selected Cytokines during Continuous Veno-Venous Hemodialysis Using High Cutoff Hemofilters in Patients with Sepsis and Acute Kidney Injury.Blood purification · 2018Article
- Selective interleukin-1 receptor-associated kinase 4 inhibitors for the treatment of autoimmune disorders and lymphoid malignancy.The Journal of experimental medicine · 2015Article
- Elevated Serum PCT in Septic Shock With Endotoxemia Is Associated With a Higher Mortality Rate.Medicine · 2015Article
- The first trimester gravid serum regulates procalcitonin expression in human macrophages skewing their phenotype in vitro.Mediators of inflammation · 2014Article
- The Role of Lipopolysaccharide-Induced Cell Signalling in Chronic Inflammation.Chronic stress (Thousand Oaks, Calif.)Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundProcalcitonin (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.
resultsPCT 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.
conclusionsThis 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.
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