Key result
IL-17A blockade reduces viral replication and inflammatory cytokines in mouse viral myocarditis.
Why the study?
The mechanism underlying the increased Th17 cell response in coxsackievirus-induced myocarditis was unclear.
Does anti-mouse IL-17Ab reduce myocardial injury and viral replication in mice with coxsackievirus B3-induced acute myocarditis?
Does anti-mouse IL-17Ab reduce myocardial injury and viral replication in mice with coxsackievirus B3-induced acute myocarditis?
Blockade of IL-17A protects against coxsackievirus B3-induced myocarditis by increasing COX-2 and PGE2 production, reducing viral replication and myocardial injury in a murine model.
IL-17A blockade merits clinical investigation in viral myocarditis; hypothesis-generating from murine evidence alone.
The Th17/interleukin (IL)-17 axis controls inflammation and might be important in the pathogenesis of experimental autoimmune myocarditis (EAM) and other autoimmune diseases. However, the mechanism underlying the increased Th17 cell response in coxsackievirus-induced myocarditis remains unclear. This study aimed to elucidate the regulatory mechanisms affected by blocking IL-17A responses in acute virus-induced myocarditis (AVMC) mice. The results showed that IL-17A and COX-2 proteins were significantly increased in the cardiac tissue of acute myocarditis, as were Th17 cells in the spleen. Using anti-mouse IL-17Ab to block IL-17A on day 7 of the viral myocarditis led to decreased expressions of cardiac tumor-necrosis factor alpha, IL-17A and transforming growth factor beta in AVMC mice compared to isotype control mice. COX-2 and prostaglandin E2 proteins were dramatically elevated, followed by marked reductions in CVB3 replication and myocardial injury. These results hint that the Th17/IL-17 axis is intimately associated with viral replication in acute myocarditis via induction of COX-2 and prostaglandin E2.
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Xie et al. (2011) studied Acute virus-induced myocarditis. Anti-mouse IL-17Ab vs. Isotype control was evaluated on Expressions of cardiac tumor-necrosis factor alpha, IL-17A, transforming growth factor beta, COX-2, prostaglandin E2, CVB3 replication, and myocardial injury. Blocking IL-17A with anti-mouse IL-17Ab in acute viral myocarditis mice decreased inflammatory cytokines and viral replication while elevating COX-2 and prostaglandin E2 proteins.
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