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Published online before print May 30, 2007
Eur Respir J 2007, doi:10.1183/09031936.00154206
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ORIGINAL ARTICLE

Suppression of endotoxin-induced inflammation by taxol

T. Mirzapoiazova 1, I.A. Kolosova 2, L. Moreno 1, S. Sammani 1, J.G.N. Garcia 1, A.D. Verin 3*

1 Dept of Medicine, The University of Chicago, Chicago, IL
2 Dept of Medicine, Case Western Reserve University, Cleveland, OH
3 Vascular Biology Center, Medical College of Georgia, Augusta, GA.

* To whom correspondence should be addressed. E-mail: averin{at}mcg.edu.


  Abstract

The pathogenesis of acute lung injury includes transendothelial diapedesis of leukocytes into lung tissues and disruption of endothelial/epithelial barriers leading to protein-rich oedema. In vitro studies show that microtubule network plays a role in the regulation of endothelial permeability as well as in neutrophil locomotion. We hypothesized that the microtubule-stabilizing agent, taxol, may attenuate inflammation and vascular leak associated with acute lung injury in vivo.

Intravenous-delivered taxol we employed a model of murine lung injury induced by intratracheal LPS administration and parameters of lung injury and inflammation assessed 18 hours after the treatment.

Intravenous-delivered taxol significantly reduced inflammatory histologic changes in lung parenchyma and parameters of LPS-induced inflammation: infiltration of proteins and inflammatory cells in bronchoalveolar lavage (BAL), lung myeloperoxidase activity, and extravasation of Evans blue albumin dye into lung tissue. Taxol alone (in the absence of LPS) had no appreciable effect on these parameters. In addition to lung proteins, intravenous taxol reduced accumulation of leukocytes in ascitic fluid in a model of LPS-induced peritonitis. Together, our data demonstrate that microtubule stabilization with taxol systemically attenuates LPS-induced inflammation and vascular leak.

Keywords:  Endotoxin, inflammation, lipopolysaccharide, lung injury, oedema, taxol




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