Accessible Unlicensed Requires Authentication Published by De Gruyter June 1, 2005

Anti-Inflammatory Effect of Pre-Elafin in Lipopolysaccharide-Induced Acute Lung Inflammation

E. Vachon, Y. Bourbonnais, C.D. Bingle, S. J. Rowe, M. F. Janelle and G. M. Tremblay
From the journal

Abstract

The aim of the present study was to evaluate the antiinflammatory activity of preelafin, an elastasespecific inhibitor, in lipopolysaccharide (LPS)induced acute lung inflammation. C57BL/6 mice were pretreated intranasally with recombinant human preelafin or vehicle only. One hour later, they were instilled intranasally with LPS (2 g/mouse). Animals were sacrificed 6 hours after LPS instillation and bronchoalveolar lavage (BAL) was performed with three 1- ml aliquots of saline. LPS induced a lung inflammation characterised by a 100-fold increase in BAL neutrophils compared to control animals (265.8±54.5 103 and 2.4±1.3 103 neutrophils/ml, respectively). Preelafin dosedependently reduced the neutrophil influx in the lung alveolar spaces by up to 84%. No elastase activity was detectable in all BAL fluids tested. Preelafin also reduced significantly LPSinduced gelatinase activity, as shown by zymography, and BAL macrophage inflammatory protein-2 (MIP-2) and KC levels, two potent neutrophil attractants and activators. Moreover, preelafin also significantly reduced mRNA levels of the three members of the IL-1 ligand family, namely IL-1α, IL-1β and IL-1 receptor antagonist (IL-1Ra), type II IL-1 receptor, and TNFα as assessed in whole lung tissue by RNase protection assay. Thus, preelafin may be considered as a potent antiinflammatory mediator.

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Published Online: 2005-06-01
Published in Print: 2002-08-27

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