Related Experiment Video
Updated: Aug 24, 2026

Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
Hemorrhage-induced acute lung injury is TLR-4 dependent
Katherine A Barsness1, John Arcaroli, Alden H Harken
1Department of Surgery, University of Colorado Health Sciences Center, 4200 E. Ninth Ave., Box C320, Denver, CO 80262, USA. katherine.barsness@uchsc.edu
Abstract:
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)-kappaB activation was independent of functional TLR-4, whereas endotoxin-induced activation of NF-kappaB 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.
Related Concept Videos
Acute Inflammation I: Inflammatory Response
Acute Inflammation III: Local and Systemic Effects
Acute Inflammation II: Cellular Phase
Acute Respiratory Failure-I
Definition: It is defined by specific criteria based on blood gas measurements. Hypoxemia happens when the partial pressure of oxygen (PaO2) falls below 60 mmHg. At the same time,...
Inhalation Anthrax
Pneumothorax-I
Pneumothorax can be even further classified as spontaneous, traumatic, and tension pneumothorax.

