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Ubiquitous expression of the calcitonin-i gene in multiple tissues in response to sepsis

Muller, B. and White, J. C. and Nylen, E. S. and Snider, R. H. and Becker, K. L. and Habener, J. F.. (2001) Ubiquitous expression of the calcitonin-i gene in multiple tissues in response to sepsis. Journal of Clinical Endocrinology and Metabolism, 86 (1). pp. 396-404.

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Official URL: http://edoc.unibas.ch/56851/

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Abstract

Calcitonin precursors (CTpr), including procalcitonin, are important markers and also potentially harmful mediators in response to microbial infections. The source and function of CTpr production in sepsis, however, remains an enigma. In the classical view, the transcription of the CT-I gene is restricted to neuroendocrine cells, in particular the C cells of the thyroid. To better understand the pathophysiology of CTpr induction in sepsis, we used an animal model analog to human sepsis, in which bacterial infection is induced in hamsters by implanting Escherichia coli pellets ip. Compared with control hamsters, levels of CTpr were elevated several fold in septic plasma and in nearly all septic hamster tissues analyzed. Unexpectedly, CT-messenger RNA was ubiquitously and uniformly expressed in multiple tissues throughout the body in response to sepsis. Notably, the transcriptional expression of CT-messenger RNA seemed more widely up-regulated in sepsis than were classical cytokines (e.g. tumor necrosis factor-alpha and interleukin-6). Our findings, which describe a potentially new mechanism of host response to a microbial infection mediated by CTpr, introduce a new pathophysiological role for the CT-I gene.
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:Oxford University Press
ISSN:0021-972X
e-ISSN:1945-7197
Note:Publication type according to Uni Basel Research Database: Journal article
Identification Number:
Last Modified:27 Nov 2017 07:25
Deposited On:27 Nov 2017 07:25

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