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

Citation
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
Citations number
31
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
158
Issue
8
Year of publication
1997
Pages
3805 - 3812
Database
ISI
SICI code
0022-1767(1997)158:8<3805:MFEITR>2.0.ZU;2-7
Abstract
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.