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Published ahead of print on April 12, 2007, doi:10.1165/rcmb.2006-0240OC

Am. J. Respir. Cell Mol. Biol., Volume 37, Number 2, August 2007, 186-192

A more recent version of this article appeared on August 1, 2007
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Submitted on July 6, 2006
Revised on April 11, 2007

Activation of the {alpha}7 nAChR Reduces Acid-Induced Acute Lung Injury in Mice and Rats

Xiao Su1*, Jae Woo Lee1, Zachary A Matthay1, Gabe Mednick1, Tokujiro Uchida2, Xiaohui Fang1, Naveen Gupta1, and Michael A Matthay1

1 University of California, Cardiovascular Research Institute, San Francisco, California, USA, 2 Department of Anesthesiology, Tokyo Medical and Dental University, Graduate School of Medicine, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: xiao.su{at}ucsf.edu.

New evidence indicates that neural mechanisms can downregulate acute inflammation. In these studies, we tested the potential role of the {alpha}7 nicotinic acetylcholine receptor ({alpha}7 nAChR) in a rodent model of acid-induced acute lung injury. We first determined that the {alpha}7 nAChR was expressed by alveolar macrophages and lung epithelial cells. Then, using an acid-induced acute lung injury mouse model, we found that nicotine, choline, and PNU-282987 (a specific {alpha}7 nAChR agonist) decreased excess lung water and lung vascular permeability, and reduced protein concentration in the bronchoalveolar lavage (BAL). Deficiency of {alpha}7 nAChR resulted in a 2-fold increase in excess lung water and lung vascular permeability. The reduction of proinflammatory cytokines (MIP-2 and TNF-{alpha}) in the BAL with nicotine probably resulted from the suppression of NF-{kappa}B activation in alveolar macrophages. The beneficial effect of nicotine was also tested in rat model of acid-induced acute lung injury in which BAL protein and RAGE, a marker of type I cell injury, were reduced by nicotine treatment. These results indicate that activation of {alpha}7 nAChR may provide a new therapeutic pathway for the treatment of acute lung injury.




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