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Statins are a family of drugs that lower cholesterol levels by inhibiting 3-hydroxy-3-methylglutaryl-CoA-reductase, a rate-limiting enzyme in the human mevalonate pathway of which cholesterol is the biosynthetic end product.1Statins also have a range of cholesterol-independent effects, including anti-inflammatory functions and antimicrobial activity. These pleiotropic effects are thought to account for the improved survival observed in statin-treated patients suffering from severe bacterial infections, such as sepsis and pneumonia.2,3,4In order to identify the mechanism involved in the protective effects of statins against infection, research studies focused on the direct effect of statins on bacteria. These studies suggest that statins have bacteriostatic effects on thein vitrogrowth of clinically important bacterial species, includingStaphylococcus aureusand Enterococci,5Streptococcus pneumoniaeandMoraxella catarrhalis,6andEscherichia coliandPseudomonas aeruginosa.7However, the concentrations used in thesein vitrostudies exceed the concentration detected in human serum during statin therapy,6suggesting thein vitrobacteriostatic effects of statins are not likely to account for the beneficial outcome of patients suffering from severe bacterial infections. |
