Document Detail


Immunoneutralization of the aminoprocalcitonin peptide of procalcitonin protects rats from lethal endotoxaemia: neuroendocrine and systemic studies.
MedLine Citation:
PMID:  20569200     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Severe sepsis and septic shock are an important cause of mortality and morbidity. These illnesses can be triggered by the bacterial endotoxin LPS (lipopolysaccharide) and pro-inflammatory cytokines, particularly TNF-α (tumour necrosis factor-α) and IL (interleukin)-1β. Severity and mortality of sepsis have also been associated with high concentrations of N-PCT (aminoprocalcitonin), a 57-amino-acid neuroendocrine peptide derived from ProCT (procalcitonin). Previous studies in a lethal model of porcine polymicrobial sepsis have revealed that immunoneutralization with IgG that is reactive to porcine N-PCT significantly improves short-term survival. To explore further the pathophysiological role of N-PCT in sepsis, we developed an antibody raised against a highly conserved amino acid sequence of human N-PCT [N-PCT-(44-57)]. This sequence differs by only one amino acid from rat N-PCT. First, we demonstrated the specificity of this antibody in a well-proven model of anorexia induced in rats by central administration of human N-PCT-(1-57). Next we explored further the therapeutic potential of anti-N-PCT-(44-57) in a rat model of lethal endotoxaemia and determined how this immunoneutralization affected LPS-induced lethality and cytokine production. We show that this specific antibody inhibited the LPS-induced early release of TNF-α and IL-1β and increased survival, even if treatment began after the cytokine response had occurred. In addition, anti-N-PCT-(44-57) may increase long-term survival in LPS-treated rats by up-regulating the late production of counter-regulatory anti-inflammatory mediators such as ACTH (adrenocorticotropic hormone) and IL-10. In conclusion, these results support N-PCT as a pro-inflammatory factor in both the early and the late stages of lethal endotoxaemia, and suggest anti-N-PCT as a candidate for septic shock therapy.
Authors:
Eva Tavares; Francisco J Miñano
Publication Detail:
Type:  Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  119     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-10-20     Completed Date:  2011-01-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  519-34     Citation Subset:  IM    
Affiliation:
Clinical and Experimental Pharmacology Research Unit, Valme University Hospital, Seville, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcitonin / genetics,  immunology*,  metabolism,  pharmacology
Cytokines / biosynthesis
Disease Models, Animal
Eating / drug effects
Endotoxemia / immunology,  metabolism,  prevention & control*
Gene Expression
Hypothalamus / metabolism
Immunotherapy / methods*
Inflammation Mediators / blood
Lipopolysaccharides
Male
Peptide Fragments / immunology
Protein Precursors / genetics,  immunology*,  metabolism,  pharmacology
Rats
Rats, Wistar
Survival Analysis
Chemical
Reg. No./Substance:
0/Cytokines; 0/Inflammation Mediators; 0/Lipopolysaccharides; 0/Peptide Fragments; 0/Protein Precursors; 56645-65-9/procalcitonin; 9007-12-9/Calcitonin
Comments/Corrections
Comment In:
Clin Sci (Lond). 2010 Dec;119(12):515-7   [PMID:  20649514 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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