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Significance Neutrophils are essential for host defense against pathogens. Although calcium signals direct numerous cell functions, the molecular machinery that orchestrates calcium influx into neutrophils is poorly defined. We demonstrate that ORAI1 and ORAI2 are key components of the mouse neutrophil calcium release-activated calcium channel and are essential for neutrophil bactericidal function. We find that neutrophils separate into two populations with distinct regulation of the membrane potential during calcium influx, which influences the magnitude of SOCE and the effect of ORAI isoform deficiency. These findings advance understanding of the mechanics of neutrophil calcium signaling, identify neutrophil subpopulations where the cell-membrane potential modulates the calcium response, and suggest mechanisms that regulate neutrophil function during infection and inflammation.

ORAI1 and ORAI2 modulate murine neutrophil calcium signaling, cellular activation, and host defense