ALTERATIONS IN FC-EPSILON-RI INDUCED BY PROTOPORPHYRIN PLUS LONG-WAVELENGTH ULTRAVIOLET-LIGHT IN MOUSE BONE-MARROW-DERIVED MAST-CELLS

As previously reported, protoporphyrin plus long-wavelength UV light ( PP/UVA) inhibits IgE-mediated degranulation of mouse bone marrow-deriv ed mast cells, as assessed by measurement of the release of beta-hexos aminidase. This inhibitory effect was seen with cells sensitized with IgE either before or after PP/UVA treatment (57.8 and 55.3% inhibition , respectively). PP/UVA did not dissociate IgE already bound to cells as assessed either by measuring release of bound I-125-IgE or by flow cytometric analysis. Results from immunoadsorption followed by SDS-PAG E analysis suggested that PP/UVA treatment may cause stable conjugatio n of IgE to its receptor. In unsensitized cells, PP/UVA did not cause conjugation of the unoccupied FcepsilonRI to other proteins in the pla sma membrane. Nevertheless, Scatchard analysis revealed that PP/UVA de creased the number of FcepsilonRI per cell by 37% (0.95 x 10(5) vs 1.5 1 x 10(5)/cell), whereas affinity of the receptor for IgE was comparab le between PP/UVA-treated and untreated cells (3.40 nM vs 3.27 nM). Fl ow cytometric analysis also confirmed the decrease in FcepsilonRI numb er in PP/UVA-treated unsensitized mouse bone marrow-derived mast cells . Although 84% of PP/UVA-treated and 82% of untreated cells expressed positive fluorescence when stained with FITC-conjugated IgE, fluoresce nce intensity was reduced by 40% after PP/UVA treatment. We conclude t hat PP/UVA alters the conformational structure and/or number of Fcepsi lonRI expressed on the mast cell surface. This effect could potentiall y explain the ability of PP/UVA to inhibit mast cell secretory functio n and may be related to an ability of PP/UVA to alter the properties o f the plasma membrane.