Abstract
The HMG-CoA reductase inhibitor Fluvastatin is a commonly used treatment for hypercholesterolemia. This drug recently has been shown to have immunological suppressive effects. Interleukin 33 (IL-33), an alarmin, has been suggested to contribute to allergies and anaphylaxis by activating mast cells. Due to the suppressive functions of Fluvastatin, we investigated the role of Fluvastatin on interleukin IL-33-stimulated mast cell function. Unlike previous studies, we have found that Fluvastatin increased production of the pro-inflammatory cytokines IL-6 and TNF-α in IL-33 stimulated mast cells. Furthermore the increase in cytokine production appeared to be stem cell factor (SCF)-dependent, since in the absence of SCF, Fluvastatin decreased cytokine production. Investigating the role of Fluvastatin in IL-33-activated mast cells will reveal a better understanding of how innate immunity may be altered by a widely-prescribed class of medications.
