MAST-CELL FC-EPSILON-RI EXPRESSION IN THE RAT INTESTINAL-MUCOSA AND TONGUE IS ENHANCED DURING NIPPOSTRONGYLUS-BRASILIENSIS INFECTION AND CAN BE UP-REGULATED BY IN-VIVO ADMINISTRATION OF IGE
N. Shaikh et al., MAST-CELL FC-EPSILON-RI EXPRESSION IN THE RAT INTESTINAL-MUCOSA AND TONGUE IS ENHANCED DURING NIPPOSTRONGYLUS-BRASILIENSIS INFECTION AND CAN BE UP-REGULATED BY IN-VIVO ADMINISTRATION OF IGE, The Journal of immunology, 158(8), 1997, pp. 3805-3812
The activation of rodent and human mast cells can occur through the cr
oss-linking of tetrameric IgE receptors each containing single alpha-
and beta- and two gamma-subunits. However, the factors that regulate t
he in vivo expression of Fc epsilon RI are poorly understood. We have
examined the expression of the Fc epsilon RI beta-subunit in the Nippo
strongylus brasiliensis (Nb)-induced model of rat intestinal inflammat
ion. We developed a double-staining technique for mast cell granules (
Alcian blue) and the beta-subunit of Fc epsilon RI. The intensity of i
mmunohistochemical staining per mast cell was quantified using an imag
e analysis system. Jejunal and tongue mast cells of Lewis rats were vi
sible by Alcian blue staining before Nb infection, but they expressed
very low levels of beta-subunit as assessed by immunohistochemical sta
ining. These levels were increased by day 11 postinfection and reached
a maximum at day 14. Since serum IgE levels correlated well with the
degree of beta-subunit expression, we investigated whether the observe
d enhancement of receptor expression might occur through the stabiliza
tion of receptor complexes by IgE. Therefore, Lewis rats were treated
with myeloma IgE, and beta-subunit expression was examined. In both to
ngue and jejunal tissue, a significant rise in beta-subunit expression
was observed in response to IgE injection, although levels of beta-su
bunit expression were not as high as those observed in Nb-infected ani
mals. The increase in beta-subunit expression was accompanied by an in
crease in the amount of mast cell-associated IgE. These observations m
ay have important implications for the regulation of IgE receptor expr
ession during disease.