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Artikel: Hypertonic Saline Suppresses NADPH Oxidase-Dependent Neutrophil Extracellular Trap Formation and Promotes Apoptosis.

Nadesalingam, Ajantha / Chen, Jacky H K / Farahvash, Armin / Khan, Meraj A

Frontiers in immunology

2018  Band 9, Seite(n) 359

Abstract: Tonicity of saline (NaCl) is important in regulating cellular functions and homeostasis. Hypertonic saline is administered to treat many inflammatory diseases, including cystic fibrosis. Excess neutrophil extracellular trap (NET) formation, or NETosis, ... ...

Abstract Tonicity of saline (NaCl) is important in regulating cellular functions and homeostasis. Hypertonic saline is administered to treat many inflammatory diseases, including cystic fibrosis. Excess neutrophil extracellular trap (NET) formation, or NETosis, is associated with many pathological conditions including chronic inflammation. Despite the known therapeutic benefits of hypertonic saline, its underlying mechanisms are not clearly understood. Therefore, we aimed to elucidate the effects of hypertonic saline in modulating NETosis. For this purpose, we purified human neutrophils and induced NETosis using agonists such as diacylglycerol mimetic phorbol myristate acetate (PMA), Gram-negative bacterial cell wall component lipopolysaccharide (LPS), calcium ionophores (A23187 and ionomycin from
Mesh-Begriff(e) Apoptosis ; Calcium Ionophores/immunology ; Cells, Cultured ; Dehydration ; Diglycerides/immunology ; Escherichia coli/physiology ; Extracellular Traps/metabolism ; Humans ; Lipopolysaccharides/immunology ; NADPH Oxidases/metabolism ; Neutrophils/physiology ; Pseudomonas aeruginosa/physiology ; Reactive Oxygen Species/metabolism ; Saline Solution, Hypertonic/metabolism ; Tetradecanoylphorbol Acetate/immunology
Chemische Substanzen Calcium Ionophores ; Diglycerides ; Lipopolysaccharides ; Reactive Oxygen Species ; Saline Solution, Hypertonic ; NADPH Oxidases (EC 1.6.3.-) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
Sprache Englisch
Erscheinungsdatum 2018-03-08
Erscheinungsland Switzerland
Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID 2606827-8
ISSN 1664-3224
ISSN 1664-3224
DOI 10.3389/fimmu.2018.00359
Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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