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Am J Physiol Regul Integr Comp Physiol 287: R592-R599, 2004. First published April 8, 2004; doi:10.1152/ajpregu.00412.2003
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INFLAMMATION AND CYTOKINES

Hemorrhage-induced acute lung injury is TLR-4 dependent

Katherine A. Barsness,1 John Arcaroli,2 Alden H. Harken,1 Edward Abraham,2 Anirban Banerjee,1 Leonid Reznikov,3 and Robert C. McIntyre1

1Department of Surgery, 2Division of Pulmonary and Critical Care Medicine, and 3Division of Infectious Diseases, University of Colorado Health Sciences Center, Denver, Colorado 80262

Submitted 23 July 2003 ; accepted in final form 1 April 2004

Toll-like receptor 4 (TLR-4), initially identified as an LPS receptor, is critical to the signaling of a variety of danger signals, including heat shock protein 60, fibrinogen, and fibronectin. Recent data also suggest that TLR-4 plays a role in determining survival in both endotoxemia and hemorrhagic shock. We hypothesized that a functional TLR-4 would be required for hemorrhage and endotoxin-induced acute lung injury. Hemorrhage- and endotoxin-induced lung TNF-{alpha} mRNA and protein production, neutrophil accumulation, and protein permeability were dependent on a functional TLR-4. Hemorrhage-induced nuclear factor (NF)-{kappa}B activation was independent of functional TLR-4, whereas endotoxin-induced activation of NF-{kappa}B requires a functional TLR-4 for full response. Therefore, we conclude that 1) hemorrhage-induced acute lung injury is TLR-4 dependent and 2) hemorrhage has a different and distinct TLR-4-dependent intracellular activation mechanism compared with endotoxemia.

endotoxin; nuclear factor-{kappa}B; tumor necrosis factor-{alpha}


Address for reprint requests and other correspondence: K. A. Barsness, 4200 E. Ninth Ave., Box C320, Denver, CO 80262 (E-mail: katherine.barsness{at}uchsc.edu)




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