Elderly susceptibility to infectious diseases results from a decline in the functions of neutrophils that are regulated by the intracellular calcium concentration [Ca+2]i and store-operated Ca+2 entry (SOCE). In this study, we analyzed the effects of aging on Ca+2 mobilization towards fMLP, IL-8, C5a, LPS, and thapsigargin (TG) as well as on chemotaxis of neutrophils. To examine Ca+2 mobilization, neutrophils from healthy elderly and young adults were loaded with 1 µM Fluo-4-AM. Baseline [Ca+2]i level was recorded for 60 seconds before the addition of 100 nM or 1µM fMLP, 300nM IL-8, 10nM C5a, 25µg/ml LPS or 2 µM TG, responses were recorded 10 min. Chemotaxis towards 10 nM fMLP, 1 nM and 10 nM C5a or IL-8 was measured by transwell migration assay for 2 h at 37 C in 5% CO2. Both assays were analyzed by flow cytometry. We found lower baseline [Ca+2]i in neutrophils from elderly. C5a, IL-8 and fMLP induced a transient peak of Ca+2followed by a second minor Ca+2 wave. However, in neutrophils from elderly, the second Ca+2 wave was lower with C5a, and higher with IL-8 and fMLP. We did not find significant difference in Ca+2 responses to LPS and TG (SOCE), as well as in the expression of stimulus receptors (CD88, CXCR2, FPLR1 and TRL4). Finally, we found that neutrophils from elderly migrated less towards fMLP, IL-8 and C5a. Our data suggest that the mechanisms that underlie the decrease on neutrophil functions with aging might be alterations in Ca+2 signals.