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Am J Physiol Regul Integr Comp Physiol (April 8, 2004). doi:10.1152/ajpregu.00412.2003
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Submitted on July 23, 2003
Accepted on April 1, 2004

Hemorrhage-Induced Acute Lung Injury is TLR-4 Dependent

Katherine A Barsness1*, John Arcaroli2, Alden H Harken1, Edward Abraham2, Anirban Banerjee1, Leonid Reznikov3, and Robert C McIntyre, Jr.1

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

* To whom correspondence should be addressed. E-mail: katherine.barsness{at}uchsc.edu.

Toll-like receptor 4 (TLR-4), initially identified as a 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. Results: 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 NF-{kappa}B activation was independent of functional TLR-4, while 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 to endotoxemia.




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