This study was published in the Journal of Leukocyte Biology 2010 Mar;87(3):433-42
Study title and authors:
Opposite effects of simvastatin on the bactericidal and inflammatory response of macrophages to opsonized S. aureus.
Benati D, Ferro M, Savino MT, Ulivieri C, Schiavo E, Nuccitelli A, Pasini FL, Baldari CT.
Department of Evolutionary Biology, University of Siena, Via Aldo Moro 2, 53100 Siena, Italy.
This study can be accessed at: http://www.ncbi.nlm.nih.gov/pubmed/19892847
Phagocytes are white blood cells that protect the body by ingesting harmful toxins, bacteria and dead and dying cells. Cytokines (Tumor necrosis factor alpha (TNFa) and Cyclooxygenase 2 (COX-2), are molecules that trigger and sustain inflammation.
Staphylococcus aureus is a bacterium that is frequently found in the human respiratory tract and on the skin. It is a common cause of skin infections (e.g. boils), respiratory disease (e.g. sinusitis), and food poisoning.
This study investigated the effects of simvastatin on the immune system. The study used human phagocytes that were pretreated with carrier or simvastatin, alone or in association with mevalonate, and subsequently incubated with Staphylococcus aureus.
The study found:
(a) Phagocyte activity was blocked by simvastatin. This effect by simvastatin was reversed by mevalonate.
(b) TNFa and COX-2 activity was enhanced by simvastatin compared with carrier-treated controls. This effect by simvastatin was reversed by mevalonate.
(c) Mevalonate is inhibited by statins.
The results of the study show that statins impair the ability of phagocytes to kill dangerous pathogens, but enhance the production of cytokines that cause excessive inflammation.
Benati concludes: "By enhancing TNFa and COX-2 production while impairing the mechanisms responsible for bacterial killing in macrophages exposed to opsonized bacteria, simvastatin may contribute to establish a state of undesirable, “gratuitous” inflammation in chronically treated patients".
