Mechanical ventilation augments lung inflammation resulting from exposure to microbial products.
Mechanical ventilation augments PMN recruitment, cytokine expression, and lung permeability in murine models of Staphylococcus aureus pneumonia [ 11] and viral pneumonia [ 12].
The first set of experiments demonstrated that mechanical ventilation augments TLR3-induced cytokine production, PMN recruitment, and lung permeability via one or more MyD88-dependent pathways.
We hypothesized that mechanical ventilation (MV) augmented sepsis-induced myocardial CML deposition and inflammation.
However, mechanical ventilation does augment both lung inflammation and injury in the presence of a variety of pro-inflammatory stimuli, including LPS, bacterial pneumonia, and viral pneumonia [ 9- 12].
Mechanical ventilation with hyperoxia significantly augmented the activation of Akt and eNOS at 1 hour of ventilation as compared with mechanical ventilation with normoxia.
We therefore tested whether mechanical ventilation with normal tidal volumes augmented inflammatory responses via a TLR4-dependent mechanism.
These data show that mechanical ventilation does not require TLR4 to augment lung inflammation and injury associated with TLR3 activation.
Even mechanical ventilation with moderate tidal volumes can augment the sepsis-induced lung injury by synergistically increasing lung cytokines, and may play a pivotal role in the development of acute lung injury in patients with sepsis [ 37- 40].
Using mechanical ventilation, we found the addition of hypoxia augmented phosphorylation of Akt in a time-dependent manner.
