Functional identification of the alveolar edema reabsorption activity of murine tumor necrosis factor-alpha.

Détails

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Etat: Public
Version: Final published version
ID Serval
serval:BIB_06D8EFDB0E69
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Functional identification of the alveolar edema reabsorption activity of murine tumor necrosis factor-alpha.
Périodique
American Journal of Respiratory and Critical Care Medicine
Auteur(s)
Elia N., Tapponnier M., Matthay M.A., Hamacher J., Pache J.C., Brundler M.A., Totsch M., De Baetselier P., Fransen L., Fukuda N., Morel D.R., Lucas R.
ISSN
1073-449X (Print)
ISSN-L
1073-449X
Statut éditorial
Publié
Date de publication
2003
Volume
168
Numéro
9
Pages
1043-1050
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
Publication Status: ppublish
Résumé
Tumor necrosis factor-alpha (TNF-alpha) activates sodium channels in Type II alveolar epithelial cells, an important mechanism for the reported fluid resorption capacity of the cytokine. Both TNF-alpha receptor-dependent and -independent effects were proposed for this activity in vitro, the latter mechanism mediated by the lectin-like domain of the molecule. In this study, the relative contribution of the receptor-dependent versus receptor-independent activities was investigated in an in situ mouse lung model and an ex vivo rat lung model. Fluid resorption due to murine TNF-alpha (mTNF-alpha) was functional in mice that were genetically deficient in both types of mTNF-alpha receptor, establishing the importance of mTNF-alpha receptor-independent effects in this species. In addition, we assessed the capacity of an mTNF-alpha-derived peptide (mLtip), which activates sodium transport by a receptor-independent mechanism, to reduce lung water content in an isolated, ventilated, autologous blood-perfused rat lung model. The results show that in this model, mLtip, in contrast to mTNF-alpha, produced a progressive recovery of dynamic lung compliance and airway resistance after alveolar flooding. There was also a significant reduction in lung water. These results indicate that the receptor-independent lectin-like domain of mTNF-alpha has a potential physiological role in the resolution of alveolar edema in rats and mice.
Mots-clé
Amiloride/pharmacology, Animals, Biological Transport/physiology, Diuretics/pharmacology, Female, Lung/pathology, Male, Mice, Mice, Inbred C57BL, Models, Animal, Organ Size, Peptide Fragments/metabolism, Pulmonary Edema/metabolism, Rats, Rats, Sprague-Dawley, Receptors, Tumor Necrosis Factor/deficiency, Receptors, Tumor Necrosis Factor/metabolism, Respiratory Mechanics/drug effects, Sodium Channels/drug effects, Sodium Channels/metabolism, Tumor Necrosis Factor-alpha/metabolism
Pubmed
Web of science
Création de la notice
19/10/2016 14:23
Dernière modification de la notice
06/10/2019 6:08
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