Abstract
Abstract Up-regulation of Lectin-like oxidized LDL receptor-1 (LOX-1) has been known to mediate oxidized LDL-induced vascular inflammation and atherogenesis. Even though there has been increasing evidence suggesting that LOX-1 may play an important role in chronic inflammation, the role of LOX-1 in acute inflammation and tissue injury remains largely unknown. In our present study, we assessed the role of LOX-1 in a mouse model of endotoxin-induced acute lung injury. We demonstrated that LOX-1 could act directly as a neutrophil adhesion molecule. Importantly, blockade of LOX-1 was able to inhibit neutrophil infiltration into the lung. Furthermore, LOX-1 appears to play an important role in mediating pro-inflammatory signaling. NF-κB activation, ICAM-1 expression and apoptotic signaling induced by endotoxin challenge in the lung were all significantly inhibited by LOX-1 blockade. Collectively, our results indicate that LOX-1 could be a multi-functional pro-inflammatory mediator that may play important role in both the induction and development of acute lung inflammation and injury. Our studies also suggest that LOX-1 may serve as a potential therapeutic target against septic shock.
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