Toll-like receptor 3 plays a central role in cardiac dysfunction during polymicrobial sepsis

Critical Care Medicine

Volumn 40, Issue 8, 2012, Pages 2390-2399

  Gao, Ming ^a   Ha, Tuanzhu ^a   Zhang, Xia ^a   Liu, Li ^c   Wang, Xiaohui ^a   Kelley, Jim ^a   Singh, Krishna ^b   Kao, Race ^a   Gao, Xiang ^d   Williams, David ^a   Li, Chuanfu ^a  

^a Internal Medicine   (United States)

^b East Tennessee State University   (United States)

^c THE FIRST AFFILIATED HOSPITAL OF NANJING MEDICAL UNIVERSITY   (China)

^d NANJING UNIVERSITY   (China)

Author keywords

apoptosis; cardiac function; neutrophils; sepsis; Toll like receptor 3

Indexed keywords

BETA INTERFERON; FAS ANTIGEN; FAS LIGAND; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; INTERCELLULAR ADHESION MOLECULE 1; INTERFERON REGULATORY FACTOR 3; INTERLEUKIN 1BETA; INTERLEUKIN 6; TOLL LIKE RECEPTOR 3; TOLL LIKE RECEPTOR 4; TOLL LIKE RECEPTOR ADAPTOR MOLECULE 1; TUMOR NECROSIS FACTOR ALPHA; VASCULAR CELL ADHESION MOLECULE 1;

ANIMAL EXPERIMENT; ANIMAL TISSUE; APOPTOSIS; ARTICLE; CONTROLLED STUDY; CYTOKINE PRODUCTION; CYTOKINE RELEASE; ENDOSOME; HEART DISEASE; HEART EJECTION FRACTION; MALE; MORTALITY; MOUSE; NONHUMAN; POLYMICROBIAL SEPSIS; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; SEPSIS; SIGNAL TRANSDUCTION; SURVIVAL RATE;

ANIMALS; APOPTOSIS; BLOTTING, WESTERN; ECHOCARDIOGRAPHY; ELECTROPHORETIC MOBILITY SHIFT ASSAY; HEART; MACROPHAGES; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; NEUTROPHIL INFILTRATION; NEUTROPHILS; PEROXIDASE; SEPSIS; TOLL-LIKE RECEPTOR 3;

EID: 84864284372     PISSN: 00903493     EISSN: 15300293     Source Type: Journal    
DOI: 10.1097/CCM.0b013e3182535aeb     Document Type: Article

References (27)

1. Krishnagopalan S, Kumar A, Parrillo JE, et al: Myocardial dysfunction in the patient with sepsis. Curr Opin Crit Care 2002; 8:376-388.
2. Oberholzer A, Oberholzer C, Moldawer LL: Sepsis syndromes: Understanding the role of innate and acquired immunity. Shock 2001; 16:83-96. (Pubitemid 33596740)
3. Aderem A, Ulevitch RJ: Toll-like receptors in the induction of the innate immune response. Nature 2000; 406:782-787.
4. Akira S, Takeda K: Toll-like receptor signalling. Nat Rev Immunol 2004; 4:499-511. (Pubitemid 38931765)
5. Frantz S, Ertl G, Bauersachs J: Mechanisms of disease: Toll-like receptors in cardiovascular disease. Nat Clin Pract Cardiovasc Med 2007; 4:444-454. (Pubitemid 47180328)
6. Frantz S, Kobzik L, Kim YD, et al: Toll4 (TLR4) expression in cardiac myocytes in normal and failing myocardium. J Clin Invest 1999; 104:271-280.
7. Williams DL, Ha T, Li C, et al: Modulation of tissue Toll-like receptor 2 and 4 during the early phases of polymicrobial sepsis correlates with mortality. Crit Care Med 2003; 31:1808-1818. (Pubitemid 36714241)
8. Ha T, Lu C, Liu L, et al: TLR2 ligands attenuate cardiac dysfunction in polymicrobial sepsis via a phosphoinositide 3-kinase-dependent mechanism. Am J Physiol Heart Circ Physiol 2010; 298:H984-H991.
9. Browder W, Ha T, Li C, et al: Early activation of pulmonary nuclear factor kB and nuclear factor interleukin-6 in polymicrobial sepsis. J Trauma 1999; 46:590-596. (Pubitemid 29186342)
10. Williams DL, Ha T, Li C, et al: Inhibiting early activation of tissue nuclear factor-kB and nuclear factor interleukin 6 with (1->3)-beta-D-glucan increases long-term survival in polymicrobial sepsis. Surgery 1999; 126:54-65. (Pubitemid 29340692)
11. Matsumoto M, Seya T: TLR3: interferon induction by double-stranded RNA including poly(I:C). Adv Drug Deliv Rev 2008; 60:805-812.
12. Cavassani KA, Ishii M, Wen H, et al: TLR3 is an endogenous sensor of tissue necrosis during acute inflammatory events. J Exp Med 2008; 205:2609-2621.
13. Karikó K, Ni H, Capodici J, et al: mRNA is an endogenous ligand for Toll-like receptor. J Biol Chem 2004; 279:12542-12550. (Pubitemid 38445825)
14. Sloane JA, Blitz D, Margolin Z, et al: A clear and present danger: endogenous ligands of Toll-like receptors. Neuromolecular Med 2010; 12:149-163.
15. Ha T, Hua F, Grant D, et al: Glucan phosphate attenuates cardiac dysfunction and inhibits cardiac MIF expression and apoptosis in septic mice. Am J Physiol Heart Circ Physiol 2006; 291:H1910-H1918. (Pubitemid 44497699)
16. Williams DL, Li C, Ha T, et al: Modulation of the phosphoinositide 3-kinase pathway alters innate resistance to polymicrobial sepsis. J Immunol 2004; 172:449-456. (Pubitemid 38020500)
17. Ha T, Hu Y, Liu L, et al: TLR2 ligands induce cardioprotection against ischaemia/reperfusion injury through a PI3K/Akt-dependent mechanism. CardiovascRes 2010; 87:694-703.
18. Cao Z, Hu Y, Wu W, et al: The TIR/BB-loop mimetic AS-1 protects the myocardium from ischaemia/reperfusion injury. Cardiovasc Res 2009; 84:442-451.
19. Williams DL, Ha T, Li C, et al: Early activation of hepatic NFkappaB and NF-IL6 in polymicrobial sepsis correlates with bacteremia, cytokine expression, and mortality. Ann Surg 1999; 230:95-104. (Pubitemid 30190370)
20. Alves-Filho JC, de Freitas A, Spiller F, et al: The role of neutrophils in severe sepsis. Shock 2008; 30 Suppl 1:3-9.
21. Cavaillon JM, Adib-Conquy M: Monocytes/ macrophages and sepsis. Crit Care Med 2005; 33(12 Suppl):S506-S509.
22. Davani EY, Boyd JH, Dorscheid DR, et al: Cardiac ICAM-1 mediates leukocyte-dependent decreased ventricular contractility in endotoxemic mice. Cardiovasc Res 2006; 72:134-142. (Pubitemid 44310639)
23. Sun R, Zhang Y, Lv Q, et al: Toll-like receptor 3 (TLR3) induces apoptosis via death receptors and mitochondria by up-regulating the transactivating p63 isoform alpha (tap63alpha). J Biol Chem 2011; 286:15918-15928.
24. Raeburn CD, Calkins CM, Zimmerman MA, et al: ICAM-1 and VCAM-1 mediate endotoxemic myocardial dysfunction independent of neutrophil accumulation. Am J Physiol Regul Integr Comp Physiol 2002; 283:R477-R486. (Pubitemid 34863896)
25. Rittirsch D, Flierl MA, Ward PA: Harmful molecular mechanisms in sepsis. Nat Rev Immunol 2008; 8:776-787.
26. Frangogiannis NG, Smith CW, Entman ML: The inflammatory response in myocardial infarction. Cardiovasc Res 2002; 53:31-47. (Pubitemid 34020764)
27. Binck BW, Tsen MF, Islas M, et al: Bone marrow-derived cells contribute to contractile dysfunction in endotoxic shock Am J Physiol Heart Circ Physiol 2005; 288:H577-H583 (Pubitemid 40139640)