Possible role of TNF on procalcitonin release in a baboon model of sepsis

Procalcitonin (PCT) has been described as an early and discriminating marker of bacteria-associated sepsis in patients. However, little is known of its source and actions, especially with regard to its relation to tumor necrosis factor (TNF). TNF is responsible for the release of several other media...

Full description

Saved in:
Bibliographic Details
Published in:Shock (Augusta, Ga.) Ga.), 2001-07, Vol.16 (1), p.25-27
Main Authors: REDL, Heinz, SCHIESSER, Anna, TÖGEL, Eva, ASSICOT, Marcel, BOHUON, Claude
Format: Article
Language:English
Subjects:
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Antibodies - pharmacology
Biological and medical sciences
Calcitonin - blood
Cytokines - blood
Disease Models, Animal
Emergency and intensive care: infection, septic shock
Intensive care medicine
Male
Medical sciences
Papio
Protein Precursors - blood
Sepsis - drug therapy
Sepsis - metabolism
Tumor Necrosis Factor-alpha - immunology
Tumor Necrosis Factor-alpha - metabolism
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Procalcitonin (PCT) has been described as an early and discriminating marker of bacteria-associated sepsis in patients. However, little is known of its source and actions, especially with regard to its relation to tumor necrosis factor (TNF). TNF is responsible for the release of several other mediators of sepsis e.g., chemokines. We tested the hypothesis that plasma PCT levels during sepsis differ with regard to the degree of TNF availability. Severe hyperdynamic sepsis was induced in baboons (n = 14) by i.v. infusion of live E. coli (approximately 2 x 10(9) colony-forming units/kg) over 2 h. Animals were pretreated 2 h before E. coli either with 1 mg/kg humanized anti-TNF antibody (CDP571) or placebo (Ringer solution). Plasma PCT levels at baseline was barely detectable, but increased to about 4000 pg/mL at 4 h after E. coli infusion. Levels were maximal between 8 and 24 h and had returned nearly to baseline at 72 h. Although no TNF could be measured in the treated group, PCT levels were not different between the placebo and the TNF antibody treatment group. We conclude that PCT levels are not dependent on the systemic presence of TNF in an E. coli sepsis model in baboons. Such sepsis induced PCT release is clearly different from the previously reported PCT release during infusion of rhTNF in volunteers or chimpanzees.
ISSN:1073-2322
1540-0514
DOI:10.1097/00024382-200116010-00005