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Articles in PresS, published online ahead of print August 9, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00147.2002
Submitted on May 13, 2002
Accepted on August 3, 2002
DEPENDENT MECHANISM
1 INSERM U416, Institut Pasteur, Lille, France
2 Faculte de Medecine, EA2689, IFR 22, Universite de Lille II, Lille, France
3 Hopital Saint-Louis, Service d'Anatomie et de Cytologie Pathologique, Paris, France
4 Department of Anesthesia and Perioperative Care and Surgery, University of California, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: bguery{at}invivo.edu.
Bronchial inflammation in allergic asthma is associated with active exsudation from the bronchial tree into the interstitial space of both mucosa and submucosa. The aim of this study was to evaluate epithelial and endothelial permeability as well as alveolar fluid movement in a model of chronic allergic inflammation in Brown-Norway rats sensitized and challenged with ovalbumin (OA). Controls groups were challenged with saline solution (C) and rats immunized by OA, but not challenged (Se). Lung sections showed a marked inflammatory infiltrate associated with perivascular and peribronchiolar edema in OA. To measure alveolar liquid clearance, a 5% bovine albumin solution with 1µCi of 125I-human albumin was instilled into the airspaces. Alveolar-capillary barrier permeability was evaluated by intravascular injection of 1µCi of 131I-albumin. Endothelial permeability was significantly increased in OA : from 0.08±0.01 in the C group to 0.19±0.03 in OA (p<0.05). Final to initial protein ratio was also statistically higher in OA (1.6±0.05) compared with C (1.38±0.03, p=0.01) and Se groups (1.42±0.03, p=0.04). Administration of anti-TNF-
antibodies within the instillate significantly decreased this ratio (1.32±0.08, p=0.003 vs OA). To conclude, we demonstrated a TNF- dependent increase in alveolar fluid movement in a model of severe bronchial allergic inflammation associated with endothelial and epithelial leakage.
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