Comparative transcriptomic analysis between an artificially induced SIRS in healthy individuals and spontaneous sepsis.

Autor:	Monteiro Sousa C; Novadiscovery, 60, avenue Rockefeller, 69008 Lyon, France; Université Claude Bernard Lyon 1, CNRS, UMR 5558, laboratoire de biométrie et biologie évolutive, équipe « Évaluation et modélisation des effets thérapeutiques », 7, rue Guillaume-Paradin, 69007 Lyon, France. Electronic address: claudio.ms@universite-lyon.fr., Boissel JP; Novadiscovery, 60, avenue Rockefeller, 69008 Lyon, France., Gueyffier F; Université Claude Bernard Lyon 1, CNRS, UMR 5558, laboratoire de biométrie et biologie évolutive, équipe « Évaluation et modélisation des effets thérapeutiques », 7, rue Guillaume-Paradin, 69007 Lyon, France., Olivera-Botello G; Novadiscovery, 60, avenue Rockefeller, 69008 Lyon, France.
Jazyk:	angličtina
Zdroj:	Comptes rendus biologies [C R Biol] 2015 Oct; Vol. 338 (10), pp. 635-42. Date of Electronic Publication: 2015 Aug 11.
DOI:	10.1016/j.crvi.2015.05.001
Abstrakt:	Sepsis is defined as a syndrome combining a systemic inflammatory response with a documented infection. It may progress to more serious cases such as septic shock following the failure of one or more organs and the emergence of hemodynamic defects. Assuming that the emergence of serious septic syndromes may be partially explained by the early loss of regulation of the inflammatory response, we decided to compare, in a transcriptomic perspective, the biological mechanisms expressed during an induced systemic inflammatory response with those expressed during severe septic syndromes. By using open-access transcriptomic databases, we first studied the kinetics of an induced inflammatory response. The use of functional analysis helped us identify discriminating biological mechanisms, such as the mTOR signaling pathway, between the pathological cases of sepsis and non-pathological (i.e., the artificially induced SIRS) cases. (Copyright © 2015 Académie des sciences. Published by Elsevier SAS. All rights reserved.)
Databáze:	MEDLINE
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