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Research ArticleCellular and Molecular

Regulation of Neutrophil Extracellular Trap Formation by Anti-Inflammatory Drugs

María José Lapponi, Agostina Carestia, Verónica Inés Landoni, Leonardo Rivadeneyra, Julia Etulain, Soledad Negrotto, Roberto Gabriel Pozner and Mirta Schattner
Journal of Pharmacology and Experimental Therapeutics June 2013, 345 (3) 430-437; DOI: https://doi.org/10.1124/jpet.112.202879
María José Lapponi
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Agostina Carestia
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Verónica Inés Landoni
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Leonardo Rivadeneyra
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Julia Etulain
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Soledad Negrotto
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Roberto Gabriel Pozner
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Mirta Schattner
Laboratory of Experimental Thrombosis (M.J.L., A.C., L.R., J.E., S.N., R.G.P., M.S.) and Laboratory of Physiology of Inflammatory Processes (V.I.L.), Institute of Experimental Medicine (IMEX), CONICET-National Academy of Medicine, Buenos Aires, Argentina
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Abstract

The formation of neutrophil extracellular traps (NETs) is a newly described phenomenon that increases the bacteria-killing ability and the inflammatory response of neutrophils. Because NET generation occurs in an inflammatory microenvironment, we examined its regulation by anti-inflammatory drugs. Treatment of neutrophils with dexamethasone had no effect, but acetylsalicylic acid (ASA) treatment prevented NET formation. NETosis was also abrogated by the presence of BAY 11-7082 [(E)-3-[4-methylphenylsulfonyl]-2-propenenitrile] and Ro 106-9920 [6-(phenylsulfinyl)tetrazolo[1,5-b]pyridazine], two structurally unrelated nuclear factor-κB (NF-κB) inhibitors. The decrease in NET formation mediated by ASA, BAY-11-7082, and Ro 106-9920 was correlated with a significant reduction in the phosphorylation of NF-κB p65 subunit, indicating that the activation of this transcription factor is a relevant signaling pathway involved in the generation of DNA traps. The inhibitory effect of these drugs was also observed when NET generation was induced under acidic or hyperthermic conditions, two stress signals of the inflammatory microenvironment. In a mouse peritonitis model, while pretreatment of animals with ASA or BAY 11-7082 resulted in a marked suppression of NET formation along with increased bacteremia, dexamethasone had no effect. Our results show that NETs have an important role in the local control of infection and that ASA and NF-κB blockade could be useful therapies to avoid undesired effect of persistent neutrophil activation.

Footnotes

    • Received January 9, 2013.
    • Accepted March 26, 2013.
  • This work was supported by the National Agency of Scientific and Technological Support [Grants PICT 2008-0230] and PICT 2011-0733].

  • dx.doi.org/10.1124/jpet.112.202879.

  • Copyright © 2013 by The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 345 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 345, Issue 3
1 Jun 2013
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Research ArticleCellular and Molecular

Effect of Anti-inflammatory Drugs on NET Formation

María José Lapponi, Agostina Carestia, Verónica Inés Landoni, Leonardo Rivadeneyra, Julia Etulain, Soledad Negrotto, Roberto Gabriel Pozner and Mirta Schattner
Journal of Pharmacology and Experimental Therapeutics June 1, 2013, 345 (3) 430-437; DOI: https://doi.org/10.1124/jpet.112.202879

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Research ArticleCellular and Molecular

Effect of Anti-inflammatory Drugs on NET Formation

María José Lapponi, Agostina Carestia, Verónica Inés Landoni, Leonardo Rivadeneyra, Julia Etulain, Soledad Negrotto, Roberto Gabriel Pozner and Mirta Schattner
Journal of Pharmacology and Experimental Therapeutics June 1, 2013, 345 (3) 430-437; DOI: https://doi.org/10.1124/jpet.112.202879
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