Toll-Like Receptor 2 Mediates<i>Staphylococcus aureus</i>–Induced Myocardial Dysfunction and Cytokine Production in the Heart

DOI Web Site 被引用文献1件
  • Pascal Knuefermann
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Yasushi Sakata
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • J. Scott Baker
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Chien-Hua Huang
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Kenichi Sekiguchi
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Hordur S. Hardarson
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Osamu Takeuchi
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Shizuo Akira
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.
  • Jesus G. Vallejo
    From the Department of Pediatrics (P.K., J.S.B., C.-H.H., H.S.H., J.G.V.), Section of Infectious Diseases, and the Winters Center for Heart Failure Research (P.K., Y.S., S.-H.H., K.S., J.G.V.), Baylor College of Medicine and Texas Children’s Hospital, Houston, Tex, and the Department of Host Defense (O.T., S.A.), Osaka University, Osaka, Japan.

抄録

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

収録刊行物

  • Circulation

    Circulation 110 (24), 3693-3698, 2004-12-14

    Ovid Technologies (Wolters Kluwer Health)

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