Premium
Effects of lysophospholipids on the generation of reactive oxygen species by fMLP‐ and PMA‐stimulated human neutrophils
Author(s) -
Müller Julia,
Petković Marijana,
Schiller Jürgen,
Arnold Klaus,
Reichl Sabine,
Arnhold Jürgen
Publication year - 2002
Publication title -
luminescence
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 45
eISSN - 1522-7243
pISSN - 1522-7235
DOI - 10.1002/bio.681
Subject(s) - lysophosphatidylcholine , lysophosphatidic acid , chemistry , lysophosphatidylethanolamine , nadph oxidase , reactive oxygen species , chemiluminescence , biochemistry , stimulation , respiratory burst , n formylmethionine leucyl phenylalanine , chemotaxis , membrane , biology , receptor , phospholipid , phosphatidylcholine , chromatography , endocrinology
In this study, the effects of exogenous lysophospholipids—lysophosphatidic acid, lysophosphatidylcholine, lysophosphatidylethanolamine and lysophosphatidylserine—on the kinetics of reactive oxygen species (ROS) production by human neutrophils are described. The ROS production by human neutrophils was monitored by luminol‐amplified chemiluminescence after cell stimulation with the chemotactic tripeptide, fMLP, or with the phorbol ester, PMA. The interaction of lysophospholipids with the membrane of human neutrophils was additionally tested by mass spectrometry. Lysophosphatidylcholine showed the most pronounced effect on the chemiluminescence pattern, as well as the intensity of the fMLP and PMA‐stimulated cells, whereas lysophosphatidic acid showed a slight priming effect when fMLP was used for stimulation. In the case of fMLP‐stimulated cells, lysophosphatidylcholine inhibited the first phase and enhanced the second phase of chemiluminescence, whereas the chemiluminescence of PMA‐stimulated neutrophils was inhibited in a concentration‐dependent manner. We conclude that lysophosphatidylcholine is able to interact with protein kinase C‐dependent signalling pathways leading to NADPH oxidase activation. Copyright © 2002 John Wiley & Sons, Ltd.