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Am J Physiol Heart Circ Physiol 292: H251-H258, 2007. First published August 25, 2006; doi:10.1152/ajpheart.00398.2006
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Toll-like receptor 3 is an essential component of the innate stress response in virus-induced cardiac injury

Hordur S. Hardarson,1 J. Scott Baker,1 Zhao Yang,2,* Enkhsaikhan Purevjav,2,* Chien-Hua Huang,1,3 Lena Alexopoulou,4 Na Li,1 Richard A. Flavell,5 Neil E. Bowles,2 and Jesus G. Vallejo1,3

Department of Pediatrics, Sections of 1Infectious Diseases and 2Cardiology, 3Winters Center For Heart Failure Research, Baylor College of Medicine and Texas Children’s Hospital, Houston, Texas; 4Centre d’Immunologie de Marseille-Luminy, Centre National de la Recherche Scientifique Institut National de la Santé et de la Recherche Médicale, Marseille, France; and 5Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut

Submitted 17 April 2006 ; accepted in final form 21 August 2006

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-beta 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.

Toll-like receptors; myocardial inflammation; innate immunity


Address for reprint requests and other correspondence: J. G. Vallejo, 6621 Fannin St., FC 430.09, Houston, TX 77030 (e-mail: jvallejo{at}bcm.tmc.edu)




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