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The Journal of Immunology, 2004, 173: 7115-7119.
Copyright © 2004 by The American Association of Immunologists

CUTTING EDGE

Cutting Edge: TLR4 Activation Mediates Liver Ischemia/Reperfusion Inflammatory Response via IFN Regulatory Factor 3-Dependent MyD88-Independent Pathway1

Yuan Zhai*, Xiu-da Shen*, Ryan O’Connell{dagger}, Feng Gao*, Charles Lassman{ddagger}, Ronald W. Busuttil*, Genhong Cheng{dagger} and Jerzy W. Kupiec-Weglinski2,*,{ddagger}

* Dumont-UCLA Transplant Center, Division of Liver and Pancreas Transplantation, Department of Surgery, {dagger} Department of Microbiology, Immunology, and Molecular Genetics, Molecular Biology Institute Jonsson Comprehensive Cancer Center, and {ddagger} Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095

The triggering molecular mechanism of ischemia-reperfusion injury (IRI), which in clinical settings results in excessive and detrimental inflammatory responses, remains unclear. This study analyzes the role of the TLR system in an established murine model of liver warm ischemia followed by reperfusion. By contrasting in parallel TLR knockout mice with their wild-type counterparts, we found that TLR4, but not TLR2, was specifically required in initiating the IRI cascade, as manifested by liver function (serum alanine aminotransferase levels), pathology, and local induction of proinflammatory cytokines/chemokines (TNF-{alpha}, IL-6, IFN-inducible protein 10). We then investigated the downstream signaling pathway of TLR4 activation. Our results show that IFN regulatory factor 3, but not MyD88, mediated IRI-induced TLR4 activation leading to liver inflammation and hepatocellular damage. This study documents the selective usage of TLR in a clinically relevant noninfectious disease model, and identifies a triggering molecular mechanism in the pathophysiology of liver IRI.




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