Low-Frequency Electromagnetic Field Exposure Enhances Extracellular Trap Formation by Human Neutrophils through the NADPH Pathway

Low-frequency (LF) electromagnetic fields (EMFs) are abundantly present in modern society, and the potential biological consequences of exposure to these fields are under intense debate. Immune cells are suggested as possible target cells, though a clear mechanism is lacking. Considering their cruci...

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Bibliographic Details
Published in:Journal of innate immunity 2015-01, Vol.7 (5), p.459-465
Main Authors: Golbach, Lieke A., Scheer, Marleen H., Cuppen, Jan J.M., Savelkoul, Huub, Verburg-van Kemenade, B.M. Lidy
Format: Article
Language:English
Subjects:
Cell Line
cells
Electromagnetic Fields - adverse effects
Environmental Exposure - adverse effects
Extracellular Traps - metabolism
Humans
immunity
Immunity, Innate
macrophages
magnetic-fields
monocytes
myeloperoxidase
NADP - metabolism
NADPH Oxidases - metabolism
Neutrophils - immunology
oxidase
proliferation
Reactive Oxygen Species - metabolism
release
Research Article
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Summary:Low-frequency (LF) electromagnetic fields (EMFs) are abundantly present in modern society, and the potential biological consequences of exposure to these fields are under intense debate. Immune cells are suggested as possible target cells, though a clear mechanism is lacking. Considering their crucial role in innate immune activation, we selected an ex vivo exposure set-up with human neutrophils to investigate a possible correlation between neutrophil extracellular trap (NET) formation and LF EMF exposure. Our study shows that formation of NETs is enhanced by LF EMF exposure. Enhanced NET formation leads to increased antimicrobial properties as well as damage to surrounding cells. We found that LF-EMF-induced NET formation is dependent on the NADPH oxidase pathway and production of reactive oxygen species. Additionally, LF EMF exposure does not influence autophagy and PAD4 activity. Our study provides a mechanism by which exposure to LF EMFs could influence the innate immune system.
ISSN:1662-811X
1662-8128
DOI:10.1159/000380764