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Enhanced Superoxide Production by Rat Alveolar Macrophages Stimulated In Vitro With Biological Response Modifiers
Author(s) -
Badger Alison M.
Publication year - 1986
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.40.6.725
Subject(s) - superoxide , muramyl dipeptide , pulmonary alveolus , lymphokine , lipopolysaccharide , biology , in vitro , spleen , concanavalin a , macrophage , microbiology and biotechnology , immunology , biochemistry , enzyme
The kinetics of superoxide release and the effects of several biological response modifiers (BRM) on superoxide release from rat pulmonary alveolar macrophages (AM) have been studied. These cells produced superoxide anion both spontaneously and in repsonse to phorbol myristate acetate (PMA) in a dose‐related manner. The response to PMA peaked in approximately 2 hr and maintained plateau levels for an additional 2‐3 hr before subsiding. Pretreatment of the macrophages in vitro with a number of immunostimulants enhanced the production of superoxide above that of controls. The release of superoxide in response to the immunostimulants was a slow phenomenon that took place over a 3‐5 hr time period. Lymphokine‐containing supematants from concanavalin A (con A)‐stimulated rat spleen cells (LK‐Sup), murine recombinant gamma interferon (rMuIFN‐γ), nigeran, and muramyl dipeptide (MDP) enhanced this response in a dose‐related manner. Poly I:C and Salmonella typhosa lipopolysaccharide (LPS) stimulated rat alveolar macrophages at low but not high concentrations. In contrast to the alveolar macrophages, rat peritoneal exudate cells were not activated by immunostimulants to produce increased amounts of superoxide.