Visit our Expo - Redox and Inflammation signaling 2012

Session IX. Novel compounds targeting inflammatory signaling pathways Poster IX, 1
Oxidized phospholipids reduce the vascular leak and inflammation in the rat model of
LPS-induced acute lung injury
1Anna A. Birukova, 2Stephanie Nonas, 1Joe G.N. Garcia and 1Konstantin G. Birukov
1Department of Medicine, University of Chicago, Chicago, Illinois 60637, U.S.A. Emails:
abirukov@medicine.bsd.uchicago.edu, jgarcia@medicine.bsd.uchicago.edu,
kbirukov@medicine.bsd.uchicago.edu, 2Department of Medicine, Johns Hopkins
University, Baltimore, Maryland 21224, U.S.A. E-Mail: snonas1@jhmi.edu
Acute inflammation and vascular leak are cardinal features of acute lung injury (ALI) and the
acute respiratory distress syndrome (ARDS). Non-specific tissue inflammation and injury in
response to a variety of infectious and non-infectious insults leads to oxidative stress and the
generation lipid oxidation products. We showed that, besides antagonistic effects on toll-like
receptor 4 (TLR4) which triggers LPS-induced inflammatory cascade, oxidized 1-palmitoyl-
2-arachidonoyl-sn-glycero-3-phosphorylcholine (OxPAPC) enhances lung endothelial cell
(EC) barrier via activation of small GTPases Rac and Cdc42. Using EC cultures and rat
models of lipopolyscharide (LPS)-induced lung injury, we tested the hypothesis that OxPAPC
may affect acute lung inflammatory response to LPS and recover lung vascular barrier
properties. LPS induced 200-fold increase in broncho-alveolar lavage (BAL) cell count
(p