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Procalcitonin and proinflammatory cytokine interactions in sepsis

Whang, K. T. and Vath, S. D. and Becker, K. L. and Snider, R. H. and Nylen, E. S. and Muller, B. and Li, Q. and Tamarkin, L. and White, J. C.. (2000) Procalcitonin and proinflammatory cytokine interactions in sepsis. Shock, 14 (1). pp. 73-78.

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Official URL: http://edoc.unibas.ch/56953/

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Abstract

Immunoneutralization of procalcitonin (ProCT), a putative mediator of sepsis, has been shown to increase survival in an animal model of sepsis. To better understand the role that ProCT plays in the sepsis cascade, we studied the relationship of this hormone to the proximal proinflammatory mediators, IL-1beta and TNFalpha. Hamsters were made septic by i.p. implantation of Escherichia coli-impregnated agar pellets. A time line study of serum IL-beta, TNFalpha, and ProCT levels showed that the increase in the cytokines was transient and less than 2-fold over baseline, whereas ProCT increased <100-fold by 12 h and remains elevated through 24 h. TNFalpha (400 microg/kg) was injected into healthy animals, inducing an elevation in ProCT that was 25-fold greater than controls. ProCT (30 microg/kg) was given to healthy and septic animals. In healthy animals, there was no significant elevation in serum IL-1beta or TNFalpha levels. In septic animals, IL-1beta was modestly blunted at 3 h but not at 12 h, and there was no change in TNFalpha levels. ProCT did not initiate or enhance IL-1beta or TNFalpha expression; however, the massive and sustained elevation of this hormone seen in sepsis can be induced by the proximal cytokine, TNFalpha. This study suggests that ProCT is a secondary mediator that might augment and amplify but does not initiate the septic response. Immunoneutralization of ProCT may prove to be an important clinical strategy, in view of its sustained elevation and the difficulty in initiating therapy for sepsis during the early phases of illness.
Faculties and Departments:03 Faculty of Medicine > Bereich Medizinische Fächer (Klinik) > Allgemeine innere Medizin AG > Argovia Professur für Medizin (Müller)
03 Faculty of Medicine > Departement Klinische Forschung > Bereich Medizinische Fächer (Klinik) > Allgemeine innere Medizin AG > Argovia Professur für Medizin (Müller)
UniBasel Contributors:Müller, Beat
Item Type:Article, refereed
Article Subtype:Research Article
Publisher:Lippincott, Williams & Wilkins
ISSN:1073-2322
e-ISSN:1540-0514
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:22 Nov 2017 09:05
Deposited On:22 Nov 2017 09:05

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