Abstract
Several antibiotics are known for their ability to accumulate in neutrophils and thereby modulate the antimicrobial functions of those cells. This study demonstrates for the first time that an antibiotic, namely the fluoroquinolone enrofloxacin, enhances the formation of bovine neutrophil extracellular traps (NETs). Pharmacologically inactivated NADPH oxidase or peptidyl-arginine deiminase-4 distinctly reduced enrofloxacin-induced NET formation. Additionally, when cells were treated with cytochalasin D or nocodazole, the enrofloxacin-mediated NET induction was abolished, indicating that besides oxidative burst and histone citrullination also actin and microtubule polymerization are involved in this process.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Anti-Bacterial Agents / pharmacology*
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Cattle*
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Cells, Cultured
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Cytochalasin D / pharmacology
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Enrofloxacin
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Enzyme Inhibitors / pharmacology
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Extracellular Traps / drug effects*
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Extracellular Traps / immunology
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Fluoroquinolones / pharmacology*
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Granulocytes / drug effects*
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Granulocytes / immunology
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Histones / metabolism
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Hydrolases / antagonists & inhibitors
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Microtubules / metabolism
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NADPH Oxidases / antagonists & inhibitors
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Nocodazole / pharmacology
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Oxidation-Reduction / drug effects
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Protein Processing, Post-Translational / drug effects
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Protein-Arginine Deiminase Type 4
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Protein-Arginine Deiminases
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Tubulin Modulators / pharmacology
Substances
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Anti-Bacterial Agents
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Enzyme Inhibitors
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Fluoroquinolones
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Histones
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Tubulin Modulators
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Cytochalasin D
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Enrofloxacin
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NADPH Oxidases
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Hydrolases
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Protein-Arginine Deiminase Type 4
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Protein-Arginine Deiminases
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Nocodazole