RESUMEN
Since formyl peptide receptor 2 (FPR2) plays a key role in the regulation of innate immune response and inflammation, it has been a hot topic to develop molecules which inhibit FPR2-induced cellular responses. In this study, we investigated the effect of an FPR2-derived pepducin in human neutrophils and human umbilical vein endothelial cells (HUVECs). The pepducin (F2pal-12) selectively inhibited FPR2 agonists (MMK-1 and serum amyloid A)-stimulated neutrophil chemotaxis. MMK-1-stimulated superoxide anion production was also inhibited by F2pal-12. HUVECs also express FPR2; FPR2 agonists-stimulated HUVECs migration and tube formation were also selectively inhibited by F2pal-12 but not by scrambled control pepducin. Since FPR2 mediates inflammatory response by inducing chemotactic migration of inflammatory cells, F2pal-12 can be used as a useful material to modulate FPR2-mediated inflammatory responses.