Enterovirus-induced myocardial injury can lead to severe heart failure. To date, little is known about the early innate stress response that contributes to host defense in the heart. Toll-like receptor 3 (TLR3) is important in the initiation of the innate antiviral response. We investigated the involvement of TLR3, which recognizes viral double-stranded RNA, on encephalomyocarditis virus (EMCV) infection. To examine the contribution of TLR3 in protection from EMCV infection, we infected mice deficient in TLR3 with 50 plaque-forming units of EMCV. TLR3-deficient (TLR3−/−) mice were more susceptible to EMCV infection and had a significantly higher viral load in the heart compared with TLR3+/+ mice. Histopathological examination showed that the inflammatory changes of the myocardium were less marked in TLR3−/− than in TLR3+/+mice. TLR3−/− mice had impaired proinflammatory cytokine and chemokine expression in the heart following EMCV infection. However, the expression of interferon-β was not impaired in EMCV-infected TLR3−/− mice. EMCV infection leads to a TLR3-dependent innate stress response, which is involved in mediating protection against virus-induced myocardial injury.

Background-Staphylococcus aureus sepsis is associated with significant myocardial dysfunction. Toll-like receptor 2 (TLR2) mediates the inflammatory response to S aureus and may trigger an innate immune response in the heart. We hypothesized that a TLR2 deficiency would attenuate S aureus-induced cardiac proinflammatory mediator production and the development of cardiac dysfunction. Methods and Results-Wild-type and TLR2-deficient (TLR2D) mice were studied. S aureus challenge significantly increased tumor necrosis factor, interleukin-1␤, and nitric oxide expression in hearts of wild-type mice. This response was significantly blunted in TLR2D mice. Hearts from TLR2D mice had impaired S aureus-induced activation of interleukin-1 receptor-associated kinase, c-Jun NH 2 terminal kinase, nuclear factor-B, and activator protein-1. Moreover, hearts from TLR2D mice were protected against S aureus-induced contractile dysfunction. Conclusions-These results show for the first time that TLR2 signaling contributes to the loss of myocardial contractility and cytokine production in the heart during S aureus sepsis.

Material Serum, 1 mL anti-Borrelia burgdorferi-IgG (Elisa) anti-Borrelia burgdorferi-IgM (Elisa) anti-Borrelia burgdorferi-IgG (WB) anti-Borrelia burgdorferi-IgM (WB) Liquor, 1 mL anti-Borrelia burgdorferi-IgG (Elisa) anti-Borrelia burgdorferi-IgM (Elisa) anti-Borrelia burgdorferi-IgG (WB) anti-Borrelia burgdorferi-IgM (WB)

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