{'fraction_non_alphanumeric': 0.05741983594332588, 'fraction_numerical': 0.02609992542878449, 'mean_word_length': 5.643564356435643, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
A cytosolic calcium transient is not necessary for degranulation or oxidative burst in immune complex‐stimulated neutrophils

Receptor‐mediated activation of neutrophils (PMN) initiates possibly interdependent events, including a rapid transient increase in [Ca2+]i, implicated as a second messenger. To investigate whether this transient is required for eventual degranulation, PMN were incubated with an intracellular Ca2+ chelator (BAPTA), then exposed to chemotactic peptide [N‐formyl‐methionyl‐leucyl‐phenylalanine (fMLP)] with or without cytochalasin B (CB) or to high‐valency immune complexes (HIC); δ[Ca2+]i, δpHi, oxidative burst, and elastase release were then evaluated (plus or minus EGTA 15 s before stimulation) after 2 and 15 min incubation in 0.9 mM Ca2+. With either fMLP plus CB or HIC stimulation, BAPTA‐treated cells were unable to achieve a Ca2+ transient with a 2‐min incubation, whereas a 15‐min incubation allowed the BAPTA‐treated cells to recover a portion of the δ[Ca2+]i. Even though BAPTA‐treated cells were unable to mount a δ[Ca2+]i at 2 min, HIC‐stimulated BAPTA‐treated cells were able to elicit an oxidative burst (33% of control) and degranulation (67% of control). Therefore, we conclude that δ[Ca2+]i modulates but is not required for oxidative burst or degranulation. J. Leukoc. Biol. 62: 329–340; 1997.