The activation of rodent and human mast cells can occur through the cross-linking of tetrameric
IgE receptors each containing single alpha- and beta- and two gamma-subunits. However, the factors that regulate the in vivo expression of Fc epsilonRI are poorly understood. We have examined the expression of the Fc epsilonRI beta-subunit in the Nippostrongylus brasiliensis (Nb)-induced mode l of rat intestinal
inflammation. We developed a double-staining technique for mast cell granules (
Alcian blue) and the beta-subunit of Fc epsilonRI. The intensity of immunohistochemical staining per mast cell was quantified using an image analysis system. Jejunal and tongue mast cells of Lewis rats were visible by
Alcian blue staining before Nb
infection, but they expressed very low levels of beta-subunit as assessed by immunohistochemical staining. 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 observed enhancement of receptor expression might occur through the stabilization of receptor complexes by
IgE. Therefore, Lewis rats were treated with myeloma
IgE, and beta-subunit expression was examined. In both tongue and jejunal tissue, a significant rise in beta-subunit expression was observed in response to
IgE injection, although levels of beta-subunit expression were not as high as those observed in Nb-infected animals. The increase in beta-subunit expression was accompanied by an increase in the amount of mast cell-associated
IgE. These observations may have important implications for the regulation of
IgE receptor expression during disease.