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Neutrophils express several G-protein coupled receptors (GPCRs) and they cross regulate each other. We described a novel cross-talk mechanism in neutrophils, by which signals generated by the receptor for ATP (P2Y2) reactivate desensitized formyl peptide receptors (FPRs) so that these ligand-bound inactive FPRs resume signaling. At the signaling level, the cross-talk was unidirectional, i.e., P2Y2 ligation reactivated FPR, but not vice versa and was sensitive to the phosphatase inhibitor calyculinA. Further, we show that the cross talk between P2Y2 and FPR bypassed cytosolic Ca2+ transients and did not rely on the actin cytoskeleton. In summary, our data demonstrate a novel cross-talk mechanism that results in reactivation of desensitized FPRs and, an amplification of the neutrophil response to ATP.
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•ATP triggers the superoxide production in FPR1 desensitized but not naïve neutrophils.•The ATP response in FPR1 desensitized cells is mediated through P2Y2 and involves a reactivation of FPR1.•A novel receptor cross-talk mechanism is disclosed between FPR1 and P2Y2 in amplification of the neutrophil response to ATP.