help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Landes, R. R.
Right arrow Articles by Morrison, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Landes, R. R.
Right arrow Articles by Morrison, D. C.

American Journal of Pathology, Vol 104, 196-205, Copyright © 1981 by American Society for Investigative Pathology

REGULAR ARTICLES

Biochemical mechanisms of lipid-A-mediated enhancement of platelet secretory responses to aggregated immunoglobulins

RR Landes and DC Morrison

The mechanism by which endotoxins enhance the secretory response of washed preparations of human platelets to aggregated immunoglobulins (Agg-HGG) has been examined. Preparations of endotoxins from several rough mutants of bacteria enhance, by approximately 50-fold, the release of serotonin initiated by Agg-HGG. Endotoxins from smooth strains do not manifest this enhancement, and all endotoxin preparations are completely inactive in the absence of Agg-HGG. Preincubation and wash experiments have demonstrated that the critical initial interaction is the formation of complexes between the endotoxin and the Agg-HGG stimulus and is not dependent on an initial endotoxin- platelet interaction. Pretreatment of platelets with substimulatory concentrations of Agg-HGG, followed by the addition of endotoxin, causes a temporal decay in the degree of endotoxin-induced enhancement, which is inversely related to the concentration of Agg-HGG. This stimulus-specific desensitization suggests that the endotoxin-Agg-HGG complexes initiate release by a pathway similar to that initiated by Agg-HGG alone. We postulate that the endotoxin either enhances or stabilizes a localized platelet membrane perturbation or deformation, initiated by the Agg-HGG stimulus.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1981 by the American Society for Investigative Pathology.