Complement peptide C3a inhibits IgEmediated triggering of rat mucosal mast cells

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Abstract
The relationship between mast cells' secretory response to stimulation via their type 1 Fcε receptors (FcεRI) and that provided by the C3a fragment of the complement system was Investigated in the rat mucosal-type mast cell line RBL-2H3. These cells are known to be unresponsive to the so-called ‘peptidergic’ stimulus provided by cationlc agents, such as anaphylatoxlns, neuropeptides or polyamines. We now observed that C3a effectively inhibits the FceRI clustering Induced secretion of RBL-2H3 cells. This inhibition is dose-dependent and takes place at a C3a concentration range of 0.4–12.5 nM, I.e. at least three orders of magnitude lower than those where this anaphylatoxln exerts its secretory stimulus to ‘serosal’ mast cells. In order to identify where C3a interferes In the FceRI coupling cascade, we have studied its effect on the cells' protein phosphorylatlon pattern, hydrolysis of phosphatldyl Inositides, transient rise in free cytosollc Ca2+ Ion concentration and Ca2+ uptake. All these processes were found to be inhibited by a similar C3a concentration range.

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