The Role of Formylpeptide Receptors, C5a Receptors, and Cytosolic-Free Calcium in Neutrophil Priming

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Abstract
Polymorphonuclear leukocytes (PMNL) exposed to chemoattractants or cytokines change their functional capacity. The effect of endotoxin-activated serum as a priming agent on humanPMNL was tested. PretreatmentofPMNL with endotoxin-activated serum increased their oxidative burst in response to formylpeptide (FMLP) (P<.02)and CSa (P<.05). Priming for membrane depolarization was observed in PMNL preincubated with either endotoxin-activated serum, low concentrations of purified C5a, or endotoxin but not with decomplemented plasma. Primed PMNL had an increased number of FMLP but not C5a receptors as compared with control PMNL. The “resting” cytosolic freecalcium was increased in primed PMNL (P<.02). Intracellular calcium buffering abolished the priming effect of endotoxin-activated serum. Thus, endotoxin-activated serum can prime cellular responsiveness for membrane depolarization and superoxide production in response to FMLP and to C5a. Priming may be due to an increased resting cytosolic-free calcium.