Role of Ca2 in neutrophil function

Several lines of independent evidence point to a role for Ca2+ in the activation of the NADPH oxidase by some agonists  

However, intracellular Ca2+ increases in themselves are insufficient to activate the oxidase because levels of this cation can be artificially increased in the absence of oxidase activity (e.g. by the addition of Ca2+ iono-phores such as ionomycin). Furthermore, activation of the oxidase by agonists such as PMA occurs in the absence of intracellular Ca2+ increases. Thus, if DAG is generated at sufficiently high concentrations to activate protein kinase C, then increases in intracellular Ca2+ are not required for oxidase activation. Furthermore, some agonists (e.g. LTB4 and PAF) generate substantial increases in intracellular Ca2+ but are poor activators of the respiratory burst. Also, there is a marked discrepancy between the concentrations of some agonists (e.g. fMet-Leu-Phe) required to activate either Ca2+ increases or oxidase activity. For example, maximal elevations in Ca2+ can occur at concentrations of fMet-Leu-Phe that are too low to activate the respiratory burst. It therefore appears that intracellular Ca2+ increases are not required to activate the respiratory burst per se, but are involved in the 

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