| First Author | Knuefermann P | Year | 2004 |
| Journal | Circulation | Volume | 110 |
| Issue | 24 | Pages | 3693-8 |
| PubMed ID | 15569836 | Mgi Jnum | J:112844 |
| Mgi Id | MGI:3663827 | Doi | 10.1161/01.CIR.0000143081.13042.04 |
| Citation | Knuefermann P, et al. (2004) Toll-like receptor 2 mediates Staphylococcus aureus-induced myocardial dysfunction and cytokine production in the heart. Circulation 110(24):3693-8 |
| abstractText | 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-1beta, 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 NH2 terminal kinase, nuclear factor-kappaB, 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. |
