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The liver in sepsis: patterns of response and injury

Bauer, Michaela; Press, Adrian T.a; Trauner, Michaelb

Current Opinion in Critical Care: April 2013 - Volume 19 - Issue 2 - p 123–127
doi: 10.1097/MCC.0b013e32835eba6d

Purpose of review Sepsis elicits profound changes in the concentrations of plasma proteins synthesized by liver parenchymal cells referred to as acute-phase proteins. Mechanisms controlling this orchestrated response include release of cytokines that induce acute-phase proteins, while other ‘house-keeping’ genes are downregulated.

Recent findings Although some acute-phase proteins help to control damage, functions of many other acute-phase reactants remain obscure. Changes in acute-phase gene expression are primarily subject to transcriptional regulation and can be comprehensively monitored by array techniques. Emerging evidence from such strategies implies that in addition to a ‘common host response’ also highly specific pathways are induced in specific disease contexts. Applying a systems biology approach to the integrated response of the hepatocyte to infection would suggest that the reprogramming of metabolic functions occurs in parallel with a severity-dependent disruption of phase I and II biotransformation and canalicular transport, that is, excretory failure. Although traditionally bilirubin serves to monitor excretion, emerging evidence suggests that bile acids indicate liver dysfunction with higher sensitivity and specificity.

Summary Sepsis induces reprogramming of the hepatic transcriptome. This includes induction of adaptive acute-phase proteins but also repression of phase I, II metabolism and transport with important implications for monitoring and pharmacotherapy.

aCenter for Sepsis Control and Care, Jena University Hospital, Jena, Germany

bDivision of Gastroenterology and Hepatology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria

Correspondence to Michael Bauer, Jena University Hospital, Erlanger Allee 101, D-07747 Jena, Germany. Tel: +49 3641 9323111; e-mail:

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins