Titre
Decreased alveolar oxygen induces lung inflammation.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Auteur(s)
Madjdpour, C.
Auteure/Auteur
Jewell, U.R.
Auteure/Auteur
Kneller, S.
Auteure/Auteur
Ziegler, U.
Auteure/Auteur
Schwendener, R.
Auteure/Auteur
Booy, C.
Auteure/Auteur
Kläusli, L.
Auteure/Auteur
Pasch, T.
Auteure/Auteur
Schimmer, R.C.
Auteure/Auteur
Beck-Schimmer, B.
Auteure/Auteur
Liens vers les unités
ISSN
1040-0605
Statut éditorial
Publié
Date de publication
2003
Volume
284
Numéro
2
Première page
360
Dernière page/numéro d’article
367
Langue
anglais
Notes
Publication types: Journal Article
Résumé
Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well defined. Therefore, effects of alveolar hypoxia were studied in rat lungs, exposing rats to 10% oxygen over periods of 1, 2, 4, 6, and 8 h. An increase in the number of macrophages in bronchoalveolar lavage fluid of hypoxic animals was shown between 1 and 8 h. Extravasation of albumin was enhanced after 1 h and remained increased throughout the study period. NF-kappaB-binding activity as well as mRNA for TNF-alpha, macrophage inflammatory protein (MIP)-1beta, and monocyte chemoattractant protein (MCP)-1 were increased within the first 2 h of exposure to hypoxia. Hypoxia-inducible factor (HIF)-1alpha and intercellular adhesion molecule (ICAM)-1 mRNA were upregulated between 1 and 6 h. Elimination of alveolar macrophages by intratracheal application of liposome-encapsulated clodronate led to a decreased expression of NF-kappaB binding activity, HIF-1alpha, TNF-alpha, ICAM-1, and MIP-1beta. In summary, alveolar hypoxia induced macrophage recruitment, an increase in albumin leakage, and enhanced expression of inflammatory mediators, which were mainly macrophage dependent. Alveolar macrophages appear to have a prominent role in the inflammatory response in hypoxia-induced lung injury and the related upregulation of inflammatory mediators.
Sujets
PID Serval
serval:BIB_27710
PMID
Date de création
2007-11-19T11:24:40.714Z
Date de création dans IRIS
2025-05-20T18:44:36Z