COMPLEMENT PEPTIDES AND MAST-CELL TRIGGERING

Mucosal type mast cells have been earlier shown to be unresponsive to the so called 'peptidergic' stimulus provided by cationic agents, such as anaphylatoxins, neuropeptides or polyamines. We studied the relati onship between mast cells' secretory response to stimulation via their type 1 Fc epsilon receptors (Fc epsilon RI) and that provided by C5a and C3a fragments of the complement system, in the rat mucosal-type ma st cell line RBL-2H3. Our results shown here reveal a novel function o f C3a, its inhibitory capacity on IgE-mediated triggering of mucosal m ast cells. This activity of C3a is most probably mediated by its inter action with the beta-chain of Fc epsilon RI. While connective tissue t ype mast cells are known to be activated by micromolar concentrations of the complement peptides C3a and C5a, the amount of C3a necessary fo r the inhibition of antigen-induced degranulation of mucosal cells in our assays is in the nanomolar range. Interestingly, the other anaphyl atoxic peptide C5a, which is known to be much more effective in severa l biological assays, did not show any activity in the same test-system . (C) 1996 Elsevier Science B.V.