Abstract
Calcium flux is a critical component of neutrophil (PMN) inflammatory signaling pathways. Sphingosine kinase (SK), in turn, has been implicated in calcium signaling. G-protein coupled receptor (GPCR) ligation has been shown to activate sphingosine kinase in PMNs. C5a, an anaphylatoxin that binds to a GPCR, activates pro-inflammatory pathways in PMNs. However, its mechanism of action at priming doses has not been elucidated. We hypothesized that C5a priming recruits sphingosine kinase to the plasma membrane where it contributes to C5a induced calcium flux and priming of the NADPH oxidase.
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