Abstract
Abstract Myocarditis is an inflammatory disease of the myocardium and a major cause of sudden death in young adults. It is characterized by the presence of immune infiltrates in the myocardium and often progresses to dilated cardiomyopathy (DCM). Despite the inflammatory nature of this autoimmune disease, immunosuppressive treatments with glucocorticoids (GCs) such as dexamethasone (Dex) have not been very effective in preventing myocarditis and progression to DCM. In addition, some patients develop resistance to GCs. We hypothesized that macrophage migration inhibitory factor (MIF) may play a role in resistance to GCs, as it is the only known pro-inflammatory cytokine to be induced by GCs. Importantly, MIF counter-regulates GC-mediated immunosuppression. Using the experimental autoimmune myocarditis (EAM) model, we observed that MIF-/- mice treated with Dex were highly resistant to disease and progression to DCM. In addition, we observe lower expression of CCL3 mRNA in MIF-/- mice treated with Dex compared with wild-type mice during the onset of EAM, which indicates that MIF promotes recruitment of inflammatory cells to the myocardium. Our results suggest that therapeutic inhibition of MIF may increase the efficacy of GC treatment. This study will allow us to better understand the mechanism by which MIF affects treatment of myocarditis by inhibiting the therapeutic effects of GCs.
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