Hyperoxia induces platelet activation and lung sequestration: an event dependent on tumor necrosis factor-alpha and CD11a.

Détails

ID Serval
serval:BIB_1CBF7491D1DE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Hyperoxia induces platelet activation and lung sequestration: an event dependent on tumor necrosis factor-alpha and CD11a.
Périodique
American Journal of Respiratory Cell and Molecular Biology
Auteur(s)
Barazzone C., Tacchini-Cottier F., Vesin C., Rochat A.F., Piguet P.F.
ISSN
1044-1549 (Print)
ISSN-L
1044-1549
Statut éditorial
Publié
Date de publication
1996
Volume
15
Numéro
1
Pages
107-114
Langue
anglais
Résumé
Mice were exposed to pure oxygen for various times to explore the pulmonary platelet trapping associated with alveolar damage, its mechanism, and its role in the lesions. Platelet sequestration, evaluated by electron microscopy and by injection of radiolabeled platelets, was detectable after 72 h and reached a maximum after 96 h of exposure (i.e., shortly before death). Circulating platelets (analyzed by Facscan) showed some increase in the expression of CD11a and CD62, but little change in CD31 and CD61. Both platelet activation and lung sequestration were dependent on TNF-alpha, since antibody against TNF-alpha reduced the expression of CD11a on circulating platelets and their sequestration in the lung. Lung platelet sequestration was also decreased by anti-CD11a MoAb. Northern blot analysis of lung mRNA isolated at 96 h of oxygen exposure revealed a 7-fold increase in CD54 (intercellular adhesion molecule-1 [ICAM-1]) and a 2.5-fold increase in TNF-alpha mRNAs respectively. These results demonstrate that the platelet pulmonary trapping induced by hyperoxia is dependent upon TNF-alpha and the CD11a-CD54 adhesion molecules. However, platelet trapping does not appear to play an important pathogenic role in acute oxygen injury, since treatments that decrease trapping (anti-TNF-alpha, anti-CD11a, or antibody-induced thrombocytopenia) did not markedly attenuate the alveolar damage.
Mots-clé
Animals, Antibodies, Monoclonal, Antigens, CD18/immunology, Bronchopulmonary Sequestration/etiology, Flow Cytometry, Hyperoxia/complications, Hyperoxia/physiopathology, Intercellular Adhesion Molecule-1/genetics, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Neutrophils/physiology, Oxygen/toxicity, Platelet Activation/physiology, Pulmonary Alveoli/cytology, Pulmonary Alveoli/immunology, RNA, Messenger/analysis, Thrombocytopenia/physiopathology, Time Factors, Tumor Necrosis Factor-alpha/antagonists & inhibitors, Tumor Necrosis Factor-alpha/genetics
Pubmed
Web of science
Création de la notice
24/01/2008 16:09
Dernière modification de la notice
20/08/2019 13:53
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