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Platelets and ATP Prime Neutrophils for Enhanced O 2 ‐ Generation at Low Concentrations but Inhibit O 2 ‐ Generation at High Concentration
Author(s) -
Naum Chris C.,
Kaplan Sandra S.,
Basford R.E.
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.49.1.83
Subject(s) - platelet , superoxide , incubation , stimulation , biology , neutrophile , granulocyte , in vitro , bone marrow , priming (agriculture) , biochemistry , immunology , endocrinology , enzyme , botany , germination
Platelets are currently thought to play a role in tissue injury and inflammatory states both directly and indirectly through their action on neutrophils (PMNs). Both stimulation and inhibition of PMN superoxide anion (O 2 ‐ ) production by platelets has been reported. To clarify these discrepant observations, we investigated the effects of wide ranges of platelet to PMN ratios as well as concentrations of ATP and ADP on human PMN O 2 ‐ production. Platelets, at low platelet‐to‐PMN ratios (1:1 and 5:1), primed PMNs which were stimulated with either FMLP or PMA. However, at higher platelet‐to‐PMN ratios (25:1, 50:1, and 100:1), inhibition of O 2 ‐ production was seen. ATP also had a biphasic effect on O 2 ‐ production: low concentrations of ATP (1 x 10 ‐6 to 3.2 x 10 ‐4 M) increased O 2 production and high concentrations of ATP (6.4 x 10 ‐4 M and above) inhibited O 2 production. ADP, when added to stimulatory concentrations of ATP, also caused inhibition of O 2 ‐ production. The incubation time for platelet‐neutrophil interactions in vitro was also crucial. Short incubation periods lead to priming, whereas longer periods (> 5 min) lead to inhibition. We believe that these studies help to resolve the controversy over the effects of platelets upon the production of O 2 ‐ by human PMNs and lend further support to the notion that platelets may modulate injury resulting from neutrophil activation.