Investigation into the effects of amyloid (1-42) beta-peptide upon basal and antigen-stimulated hexosaminidase and serotonin release from rat RBL-2H3basophilic leukemia cells

There is evidence that beta -amyloid (A beta) peptide infusion in vivo prod uces a degranulation of vascular mast cells. It would be useful to investig ate the interaction between A beta and mast cells in a simple in vitro mode l system in order to determine the cellular mechanism by which exposure to A beta peptides results in mast cll degranulation. In the present study, th e effect of A beta (1-42) upon the release of granular hexosaminidase and s erotonin has been investigated using the cognate rat mast cell line, RBL-2H 3. Sensitization of these cells for 1 h with anti-DNP IgE (monoclonal anti- dinitrophenyl) results in a large release of hexosaminidase and serotonin d ue to degranulation when the cells are exposed to DNP-HSA (Albumin, human d initrophenyl). Pretreatment overnight with A beta (1-42) (10 and 30 muM) di d not affect either the basal or antigen-stimulated release of hexosaminida se or serotonin. A similar lack of effect of A beta (25-35) and the lipid p eroxidation product HNE upon antigen-stimulated release of hexosaminidase o r serotonin was also found. It is concluded that RBL-2H3 cells are not a us eful model for mechanistic studies into the effects of beta -amyloid peptid es upon vascular mast cells. (C) 2000 Prous Science. All rights reserved.