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Effects of staphylococcal enterotoxin B on rodent mast cells
1Department of Experimental Pathology, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.
Abstract:
Staphylococcal enterotoxin B (SEB) was tested in rodent mast cell cultures for the release of serotonin. Both rat RBL-2H3 mast cells and murine peritoneal cells released serotonin after SEB stimulation in culture. Release of serotonin in RBL-2H3 cells depended on the concentration of SEB; an appreciable release was seen at 50 micrograms/ml. The release of serotonin was not due to cell death. Serotonin release could be enhanced by bradykinin but not by vasoactive intestinal peptide, substance P, lipopolysaccharide from Salmonella typhimurium, the calcium ionophore A23187, acetylcholine, adenosine, 5-hydroxyeicosatetraenoic acid, indomethacin, or phorbol myristate acetate. SEB bound directly to the membrane of RBL-2H3 mast cells, and the SEB-binding site, the presumptive receptor, appeared to be a protein. The SEB receptor could not be capped under membrane-capping conditions, and serotonin release could not be enhanced by attempts to cross-link the receptor. These results suggest that mast cells may be an important cell type involved in SEB toxicosis and that release of serotonin may be enhanced by activation of the kinin-kallikrein system.
Insights
Staphylococcal enterotoxin B (SEB) triggers serotonin release from rodent mast cells. This suggests mast cells play a role in SEB toxicosis, potentially modulated by the kinin-kallikrein system.
Area of Science:
- Immunology
- Toxicology
- Cell Biology
Background:
- Staphylococcal enterotoxin B (SEB) is a potent toxin.
- Mast cells are immune cells involved in inflammatory responses.
- The role of mast cells in SEB toxicosis is not fully understood.
Purpose of the Study:
- To investigate the effect of SEB on serotonin release from rodent mast cells.
- To identify potential mechanisms and modulators of SEB-induced serotonin release.
Main Methods:
- Primary rodent mast cells (murine peritoneal cells) and a rat mast cell line (RBL-2H3) were cultured.
- Cells were stimulated with varying concentrations of SEB.
- Serotonin release was measured.
- SEB binding to mast cell membranes was assessed.
- Effects of various substances on serotonin release were tested.
Main Results:
- SEB induced serotonin release from both rat RBL-2H3 and murine peritoneal mast cells.
- Serotonin release was dose-dependent, with significant release at 50 µg/ml.
- Serotonin release was not a result of cell death.
- Bradykinin enhanced SEB-induced serotonin release, but other tested substances did not.
- SEB bound to a protein receptor on the mast cell membrane, but cross-linking did not enhance serotonin release.
Conclusions:
- Mast cells are likely involved in SEB toxicosis.
- SEB-induced serotonin release from mast cells is a key mechanism.
- The kinin-kallikrein system may enhance SEB-induced serotonin release.