Previous studies in our laboratory demonstrated the development of pulmonary inflammation in Nox2-deficient (gp91<sup>phox-/y</sup>) mice that was absent in WT mice in a murine model of SIRS.
Here, we determined whether suppression of endosome NOX2 oxidase prevents the lung inflammation following infection with a highly pathogenic IAV strain.
Inhibition of the aiPLA₂ activity and Nox2 activation of lungs in vivo was similar for intratracheal (IT) and intravenous (IV) administration of PIP-2, but required its incorporation into liposomes as a delivery vehicle; tissue ½ time for decrease of the in vivo inhibition of aiPLA₂ activity after PIP-2 administration was ~50 h. These properties suggest that PIP-2 could be an effective therapeutic agent to prevent tissue injury associated with lung inflammation.
Here we use VCAM-targeted QDs in a mouse model to show that NOX2, specifically endothelial NOX2, induces VCAM expression with lung inflammation in vivo.
These data show that P. aeruginosa lung infection up-regulates NOX2 and NOX4 expression and ROS generation, which play distinct roles in regulating lung inflammation, apoptosis, and permeability.