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Stimulus‐Specific Effects of Pentoxifylline on Neutrophil CR3 Expression, Degranulation, and Superoxide Production
Author(s) -
Currie Mark S.,
Rao K. Murali K.,
Padmanabhan Jaya,
Jones Adrie,
Crawford Jeffrey,
Cohen Harvey J.
Publication year - 1990
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.47.3.244
Subject(s) - superoxide , degranulation , pentoxifylline , cytochalasin , cytochalasin b , cytochalasin d , chemotaxis , biology , pharmacology , biochemistry , microbiology and biotechnology , receptor , cytoskeleton , in vitro , enzyme , cell
The effects of pentoxifylline (Trental) on human neutrophil CR3 up‐modulation, degranulation, and superoxide production were studied. We used the chemotactic peptide fMLP and the phorbol ester PMA as soluble stimuli, and β‐glucan particles as a CR3‐specific solid phase stimulus of neutrophil superoxide production. Since neutrophils have adenosine A 2 receptors, we compared effects of pentoxifylline to effects of adenosine, and we also looked at the effect of cytochalasin B, which breaks up actin filaments. Pentoxifylline inhibited both CR3 up‐modulation and degranulation of myeloperoxidase and lysozyme. Pentoxifylline is a more potent inhibitor of fMLP‐ compared to PMA‐induced degranulation, and is especially potent against superoxide production. While pentoxifylline is less potent than adenosine in its inhibiton of fMLP‐induced superoxide production, it is more potent in its inhibition of PMA‐ and β‐glucan particle‐stimulated superoxide production. Cytochalasin B, which enhances degranulation and fMLP‐stimulated superoxide production, was found to inhibit β‐glucan particle‐stimulated superoxide production. These findings are consistent with the hypothesis that pentoxifylline can affect both the cytoskeletal architecture of unstimulated neutrophils and the activation and responses of neutrophils which involve actin polymerization and receptor‐cytoskeletal interactions.

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