An effector role for platelets in systemic and local lipopolysaccharide-induced toxicity in mice, mediated by a CD11a- and CD54-dependent interaction with endothelium.

Détails

ID Serval
serval:BIB_AB380FE49280
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
An effector role for platelets in systemic and local lipopolysaccharide-induced toxicity in mice, mediated by a CD11a- and CD54-dependent interaction with endothelium.
Périodique
Infection and Immunity
Auteur(s)
Piguet P.F., Vesin C., Ryser J.E., Senaldi G., Grau G.E., Tacchini-Cottier F.
ISSN
0019-9567 (Print)
ISSN-L
0019-9567
Statut éditorial
Publié
Date de publication
1993
Volume
61
Numéro
10
Pages
4182-4187
Langue
anglais
Résumé
The role of platelets was investigated in two models of lipopolysaccharide (LPS)-induced toxicity in mice: the systemic reaction, provoked by intravenous LPS injection in D-galactosamine-sensitized recipients, which results in host death, and the local reaction, elicited in the skin by sequential injections of LPS and tumor necrosis factor alpha at 24-h intervals, which results in hemorrhagic necrosis. In both models, the depletion of platelets with a rabbit polyclonal or a mouse monoclonal antiplatelet immunoglobulin G afforded significant protection. In the local reaction, studies of the distribution of 111In-labelled platelets as well as optical and electron microscopy showed that platelets are localized in the dermal venules before hemorrhage occurs. Anti-CD11a (LFA-1) and anti-CD54 (ICAM-1) monoclonal antibodies prevented both platelet localization and hemorrhagic necrosis, and these determinants were detected on mouse platelets by immunofluorescence. The antiplatelet monoclonal antibody did not reduce the localization of polymorphonuclear leukocytes in the dermal venules, as shown by histological sections. Thus, in the local reaction, the stimulation with LPS and tumor necrosis factor alpha leads to a binding of platelets to the endothelium of venules by their beta 2 integrins, which seems necessary for the development of the hemorrhagic necrosis.
Mots-clé
Animals, Blood Platelets/physiology, Cell Adhesion Molecules/physiology, Endothelium, Vascular/physiopathology, Female, Galactosamine/administration & dosage, Intercellular Adhesion Molecule-1, Lipopolysaccharides/toxicity, Lymphocyte Function-Associated Antigen-1/physiology, Male, Mice, Mice, Inbred BALB C, Mice, Inbred CBA, Tumor Necrosis Factor-alpha/metabolism
Pubmed
Web of science
Création de la notice
24/01/2008 16:09
Dernière modification de la notice
20/08/2019 16:15
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