Membrane Glycoproteins in Superoxide Release from Neutrophils View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1990

AUTHORS

Giovanni Ricevuti , Antonino Mazzone , Antonia Notario

ABSTRACT

Neutrophils are the cells generally considered to be the first line of defence against invading microorganisms. Stimulation of their surface receptors activates a repertoire of killing functions as phagocytosis, superoxide production, exocytosis of acid hydrolases and proteases, chemotaxis, aggregation and generation of arachidonic acid-derived inflammatory mediators. The major microbicidal mechanisms of the human granulocytes(PMN) require the formation of reactive oxygen metabolites such as superoxide anion (02) and hydrogen peroxide (the oxidative burst) and the secretion of granule enzymes such as myeloperoxidase (degranulation). Both of these events can be triggered by various soluble or particulate stimuli which interact with the cell surface and depolarize the cell membranes. The PMN to exposed to the specific murine monoclonal antibodies (MoAbs) exhibit a significant depression in (02) generation in response to fMLP to serum-treated zymosan (STZ). Preliminary data suggested that MoAbs depolarizes the PMN cell membrane and that this may be associated with the alterations in oxidative metabolism caused by same MoAbs2’3. The purpose of this study was to explore the relationship between surface membrane glycoproteins, membrane depolarization in the human granulocytes and the subsequent oxidative burst Several MoAbs were used for to identifie the membrane glycoprotein fundamental in respiratory burst activation. More... »

PAGES

55-63

References to SciGraph publications

Book

TITLE

Free Radicals, Lipoproteins, and Membrane Lipids

ISBN

978-1-4684-7429-9
978-1-4684-7427-5

Author Affiliations

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4684-7427-5_5

DOI

http://dx.doi.org/10.1007/978-1-4684-7427-5_5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1016676151


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