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Vol. 1, No. 4, 2009
Issue release date: June 2009
Section title: Research Article
J Innate Immun 2009;1:358–365

Blockade of LOX-1 Prevents Endotoxin-Induced Acute Lung Inflammation and Injury in Mice

Zhang P.a · Liu M.-C.b · Cheng L.a · Liang M.a · Ji H.a · Fu J.a
aCenter for Biomedical Research, University of Texas Health Science Center at Tyler, Tyler, Tex., and bDepartment of Pharmacology, University of Toledo, Toledo, Ohio, USA
email Corresponding Author

Dr. Jian Fu

Department of Biochemistry, Center for Biomedical Research

University of Texas Health Science Center at Tyler

11937 US Highway 271, Tyler, TX 75708 (USA)

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Lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1), a cell surface receptor expressed in endothelial cells, is known to mediate oxidized LDL-induced vascular inflammation and atherogenesis. Although the role of LOX-1 in vascular inflammation has been well established, its involvement in acute lung inflammation and injury remains unclear. In the present study, we examined the effects of a LOX-1-blocking antibody on lung inflammation in a mouse endotoxin lipopolysaccharide (LPS)-induced acute lung injury model. We demonstrated that intraperitoneal challenge with LPS induced a rapid and robust increase in LOX-1 expression in mouse lung. Pre-treatment of mice with anti-LOX-1-blocking antibody significantly inhibited LPS-induced lung inflammation as indicated by decreased neutrophil accumulation in the lung. Furthermore, anti-LOX-1 was capable of inhibiting LPS-induced inflammatory responses, including NF-κB activation, ICAM-1 expression and apoptotic signaling, in mouse lung. Collectively, these results indicate that LOX-1 may serve as a valuable therapeutic target in the prevention of acute lung inflammation and injury in sepsis.

© 2008 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Research Article

Received: 6/16/2008
Accepted: 8/5/2008
Published online: 10/1/2008

Number of Print Pages: 8
Number of Figures: 6
Number of Tables: 0

ISSN: 1662-811X (Print)
eISSN: 1662-8128 (Online)

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