Abstract
The recruitment of neutrophils to sites of inflammation, their battle against invading microorganisms through phagocytosis and the release of antimicrobial agents is a highly coordinated and tightly regulated process that involves the interplay of many different receptors, ion channels and signalling pathways. Changes in intracellular calcium levels, caused by cytosolic Ca(2+) store depletion and the influx of extracellular Ca(2+) via ion channels, play a critical role in synchronizing neutrophil activation and function. In this review, we provide an overview of how Ca(2+) signalling is initiated in neutrophils and how changes in intracellular Ca(2+) levels modulate neutrophil function.