TY - JOUR
T1 - Mast cell activity in experimental allergic encephalomyelitis
AU - Levi-Schaffer, Francesca
AU - Riesel, Naomi
AU - Soffer, Dov
AU - Abramsky, Oded
AU - Brenner, Talma
PY - 1991/10
Y1 - 1991/10
N2 - 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.
AB - 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.
KW - B-hexosaminidase
KW - Mast cells
KW - experimental allergic encephalomyelitis
KW - nedocromil
UR - http://www.scopus.com/inward/record.url?scp=0026338068&partnerID=8YFLogxK
U2 - 10.1007/BF03159954
DO - 10.1007/BF03159954
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C2 - 1663747
AN - SCOPUS:0026338068
SN - 1044-7393
VL - 15
SP - 173
EP - 184
JO - Molecular and Chemical Neuropathology
JF - Molecular and Chemical Neuropathology
IS - 2
ER -