Serum amyloid A induces chemotaxis of human mast cells by activating a pertussis toxin-sensitive signal transduction pathway.

Serum amyloid A (SAA) is an acute-phase protein and its concentration increases in the blood up to 1000 times during an inflammatory response. Mast cells are known to accumulate in various inflammatory processes, some of which are associated with increased levels of acute-phase reactants such as SAA. We report here that SAA can act as a mast cell chemoattractant. Recombinant SAA at concentrations corresponding to those found during the acute phase induced directional migration of human mast cells. No chemokinetic effect was observed. Preincubation of the cells with pertussis toxin inhibited SAA chemotaxis, suggesting that the effect is mediated by G proteins of the Gi class. Furthermore, chemotaxis was diminished after pretreatment with genistein, a tyrosine kinase inhibitor, or bisindolylmaleimide I, a protein kinase C inhibitor. We suggest that SAA may participate in the migration of mast cells to inflamed tissues during an acute-phase response, acting through a pertussis toxin-sensitive signaling pathway. Copyright 1999 Academic Press.