Statins and sepsis: multiple modifications at multiple levels

Marius Terblanche*, Yaniv Almog, Robert Rosenson, Terry S. Smith, Daniel G. Hackam

*Corresponding author for this work

Research output: Contribution to journalLiterature reviewpeer-review

236 Citations (Scopus)

Abstract

Sepsis, an infection-induced inflammatory syndrome, is a leading and increasing cause of mortality worldwide. Animal and human observational studies suggest statins may prevent the morbidity and mortality associated with the sepsis syndrome. In this Review, we describe the demonstrated mechanisms through which statins modulate the inflammatory response associated with sepsis. These mechanisms include effects on cell signalling with consequent changes at the transcriptional level, the induction of haem oxygenase, the direct alteration of leucocyte-endothelial cell interaction, and the reduced expression of MHC II. Since statins do not target individual inflammatory mediators, but possibly reduce the overall magnitude of the systemic response, this effect could prove an important distinguishing feature modulating the host response to septic insults. This work establishes the biological plausibility needed for future trials of statins in critical illness.

Original languageEnglish
Pages (from-to)358-368
Number of pages11
JournalLancet Infectious Diseases
Volume7
Issue number5
DOIs
Publication statusPublished - May 2007

Keywords

  • C-REACTIVE PROTEIN
  • COA REDUCTASE INHIBITORS
  • HUMAN ENDOTHELIAL-CELLS
  • NITRIC-OXIDE SYNTHASE
  • VASCULAR SMOOTH-MUSCLE
  • INTENSIVE-CARE UNITS
  • POPULATION-BASED COHORT
  • NECROSIS-FACTOR-ALPHA
  • PPAR-GAMMA LIGANDS
  • NF-KAPPA-B

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