Adenosine activates Gαs proteins and inhibits C3a-induced activation of human mast cells

摘要: Anaphylatoxin C3a and adenosine receptors (AR) are implicated in the inflammatory process associated with allergic rhinitis asthma by modifying mast cell (MC) responses. Possible interactions between these G-protein coupled receptor (GPCR) pathways MCs have not yet been demonstrated. LAD2 human MC were stimulated presence or absence of AR agonists antagonists their adhesion, chemotaxis mediator release measured. The pan-specific agonist, 5'-N-Ethylcarboxamidoadenosine (NECA) inhibited C3a-induced migration, degranulation, production CCL2, ERK1/2 phosphorylation. selective A2A agonist CGS 21680 C3a-mediated while A2B A3 BAY 60-6583 IB-MECA, respectively, had no effect. Moreover, an antagonist SCH 58261 blocked inhibitory effect NECA on suggesting that inhibition degranulation was mediated through receptor. increased intracellular cAMP C3a-activated cells, Gαs protein signals required for adenosine-induced activation. adenylyl cyclase inhibitor SQ 22536 attenuated CSG potentiated activation Our results suggest inhibits possibly a protein-dependent pathway.