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Mast cell activity in experimental allergic encephalomyelitis
F Levi-Schaffer1, N Riesel, D Soffer
1Department of Pharmacology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
Abstract:
The number and functional reactivity of peritoneal mast cells (MCs) were evaluated in rats with experimental allergic encephalomyelitis (EAE). Cells were counted following staining with toluidine blue and activation was measured by B-hexosaminidase (B-hex) release. The number of detectable MCs and their capacity to release B-hex decreased significantly by 40 and 65%, respectively, as compared with normal controls just prior to the onset of clinical signs. These values returned to normal on clinical recovery. Preliminary data on MC counts performed on histological sections of rat brains with EAE suggested a similar pattern of response, i.e., an early decrease prior to disease onset with subsequent normalization on recovery. In an attempt to modify the course of EAE, rats were treated with the MC stabilizing agent nedocromil or with the MC activating agent, compound 48/80. Nedocromil induced a slight delay in the onset of EAE, but only when administered at the time of EAE induction. Compound 48/80 did not seem to affect the clinical course of the disease. Our results suggest that MCs are involved in the pathogenesis of EAE and may contribute to the induction of the disease rather than to the effector phase and its clinical expression.
Insights
Peritoneal mast cells (MCs) decrease in number and function before experimental allergic encephalomyelitis (EAE) onset in rats, suggesting MCs contribute to disease induction, not its clinical expression.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Experimental allergic encephalomyelitis (EAE) is a model for studying autoimmune CNS diseases.
- Mast cells (MCs) are immune cells known to play roles in allergic and inflammatory responses.
Purpose of the Study:
- To investigate the role of peritoneal mast cells (MCs) in the pathogenesis of experimental allergic encephalomyelitis (EAE).
- To evaluate the number and functional reactivity of MCs during different phases of EAE.
Main Methods:
- Quantification of peritoneal MCs using toluidine blue staining.
- Measurement of MC activation via B-hexosaminidase (B-hex) release.
- Histological examination of MCs in rat brain tissues.
- Pharmacological modulation of MCs using nedocromil and compound 48/80.
Main Results:
- A significant decrease (40-65%) in peritoneal MC number and B-hex release was observed prior to EAE clinical onset.
- MC levels and function normalized upon clinical recovery from EAE.
- Preliminary brain histology suggested a similar early decrease in MCs.
- Nedocromil administration delayed EAE onset slightly when given at induction; compound 48/80 had no significant effect.
Conclusions:
- Peritoneal mast cells are involved in the early stages of EAE pathogenesis.
- MCs may contribute to the induction phase of EAE rather than the effector phase.
- These findings highlight a potential role for mast cells in the initiation of autoimmune neuroinflammation.