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Published ahead of print on March 14, 2003, doi:10.1165/rcmb.2002-0132OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 2, August 2003, 252-258

A more recent version of this article appeared on August 1, 2003
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Submitted on July 29, 2002
Revised on March 14, 2003

Effect of CD14 Blockade on Endotoxin-induced Acute Lung Injury in Mice

Sadatomo Tasaka1, Akitoshi Ishizaka2*, Wakako Yamada1, Mie Shimizu1, Hidefumi Koh1, Naoki Hasegawa1, Yoshiyuki Adachi3, and Kazuhiro Yamaguchi1

1 Department of Medicine, Keio University School of Medicine, Tokyo, Japan, 2 Department of Medicine, Keio University School of Medicine, Tokyo, Japan; Department of Laboratory Medicine, Tokyo Electric Power Company Hospital, Tokyo, Japan, 3 Laboratory of Immunopharmacology of Microbial Products, Tokyo University of Pharmacy and Life Science, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: ishiz{at}attglobal.net.

CD14 functions as a cell surface receptor for endotoxin (LPS) and is thought to have an essential role in innate immune responses to infection. Previous studies have revealed attenuation of the systemic response after sepsis by blocking CD14. In this study, we tested the hypothesis that CD14 blockade protects against inflammatory responses associated with LPS pneumonia. We examined the effect of an anti-murine CD14 monoclonal antibody (4C1) on the development of acute lung injury induced by intratracheal LPS in mice. We also measured the production of cytokines (TNF-{alpha}, IL-6, and MIP-2) and nitric oxide by murine peritoneal macrophages exposed to LPS in vitro. NF-{kappa}B translocation was evaluated in nuclear extracts from lung homogenates. 4C1 significantly attenuated pulmonary edema and neutrophil emigration after LPS administration. The production of cytokines and nitric oxide by LPS-stimulated macrophages was significantly decreased by 4C1 treatment. NF-{kappa}B translocation induced by LPS instillation was also suppressed by 4C1. These results suggest that blockade of CD14 might attenuate acute lung injury after intratracheal instillation of LPS through the suppression of NF-{kappa}B translocation. The inhibitory effect of CD14 blockade on cytokine production and nitric oxide release of macrophages might contribute to the attenuation of lung injury.




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