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Aggregated neutrophil extracellular traps resolve inflammation by proteolysis of cytokines and chemokines and protection from antiproteases

J. Hahn, C. Schauer, C. Czegley, L. Kling, L. Petru, B. Schmid, D. Weidner, C. Reinwald, MHC. Biermann, S. Blunder, J. Ernst, A. Lesner, T. Bäuerle, R. Palmisano, S. Christiansen, M. Herrmann, A. Bozec, R. Gruber, G. Schett, MH. Hoffmann,

. 2019 ; 33 (1) : 1401-1414. [pub] 20180821

Language English Country United States

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc19035059

Papillon-Lefèvre syndrome (PLS) is characterized by nonfunctional neutrophil serine proteases (NSPs) and fulminant periodontal inflammation of unknown cause. Here we investigated neutrophil extracellular trap (NET)-associated aggregation and cytokine/chemokine-release/degradation by normal and NSP-deficient human and mouse granulocytes. Stimulated with solid or soluble NET inducers, normal neutrophils formed aggregates and both released and degraded cytokines/chemokines. With increasing cell density, proteolytic degradation outweighed release. Maximum output of cytokines/chemokines occurred mostly at densities between 2 × 107 and 4 × 107 neutrophils/cm3. Assessment of neutrophil density in vivo showed that these concentrations are surpassed during inflammation. Association with aggregated NETs conferred protection of neutrophil elastase against α1-antitrypsin. In contrast, eosinophils did not influence cytokine/chemokine concentrations. The proteolytic degradation of inflammatory mediators seen in NETs was abrogated in Papillon-Lefèvre syndrome (PLS) neutrophils. In summary, neutrophil-driven proteolysis of inflammatory mediators works as a built-in safeguard for inflammation. The absence of this negative feedback mechanism might be responsible for the nonresolving periodontitis seen in PLS.-Hahn, J., Schauer, C., Czegley, C., Kling, L., Petru, L., Schmid, B., Weidner, D., Reinwald, C., Biermann, M. H. C., Blunder, S., Ernst, J., Lesner, A., Bäuerle, T., Palmisano, R., Christiansen, S., Herrmann, M., Bozec, A., Gruber, R., Schett, G., Hoffmann, M. H. Aggregated neutrophil extracellular traps resolve inflammation by proteolysis of cytokines and chemokines and protection from antiproteases.

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$a Papillon-Lefèvre syndrome (PLS) is characterized by nonfunctional neutrophil serine proteases (NSPs) and fulminant periodontal inflammation of unknown cause. Here we investigated neutrophil extracellular trap (NET)-associated aggregation and cytokine/chemokine-release/degradation by normal and NSP-deficient human and mouse granulocytes. Stimulated with solid or soluble NET inducers, normal neutrophils formed aggregates and both released and degraded cytokines/chemokines. With increasing cell density, proteolytic degradation outweighed release. Maximum output of cytokines/chemokines occurred mostly at densities between 2 × 107 and 4 × 107 neutrophils/cm3. Assessment of neutrophil density in vivo showed that these concentrations are surpassed during inflammation. Association with aggregated NETs conferred protection of neutrophil elastase against α1-antitrypsin. In contrast, eosinophils did not influence cytokine/chemokine concentrations. The proteolytic degradation of inflammatory mediators seen in NETs was abrogated in Papillon-Lefèvre syndrome (PLS) neutrophils. In summary, neutrophil-driven proteolysis of inflammatory mediators works as a built-in safeguard for inflammation. The absence of this negative feedback mechanism might be responsible for the nonresolving periodontitis seen in PLS.-Hahn, J., Schauer, C., Czegley, C., Kling, L., Petru, L., Schmid, B., Weidner, D., Reinwald, C., Biermann, M. H. C., Blunder, S., Ernst, J., Lesner, A., Bäuerle, T., Palmisano, R., Christiansen, S., Herrmann, M., Bozec, A., Gruber, R., Schett, G., Hoffmann, M. H. Aggregated neutrophil extracellular traps resolve inflammation by proteolysis of cytokines and chemokines and protection from antiproteases.
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$a Schauer, Christine $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Czegley, Christine $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Kling, Lasse $u Max Planck Institute for the Science of Light, Erlangen, Germany.
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$a Petru, Lenka $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany. Department of Rheumatology, First Faculty of Medicine, Charles University-Institute of Rheumatology, Prague, Czech Republic.
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$a Schmid, Benjamin $u Optical Imaging Centre Erlangen (OICE), Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
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$a Weidner, Daniela $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Reinwald, Christiane $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Biermann, Mona H C $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Blunder, Stefan $u Department of Dermatology, Venereology, and Allergology, Medical University of Innsbruck, Innsbruck, Austria.
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$a Ernst, Jürgen $u Fraunhofer Institute for Integrated Circuits (IIS), Erlangen, Germany.
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$a Lesner, Adam $u Faculty of Chemistry, University of Gdansk, Gdansk, Poland.
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$a Bäuerle, Tobias $u Institute of Radiology, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Palmisano, Ralf $u Optical Imaging Centre Erlangen (OICE), Friedrich-Alexander-University Erlangen-Nürnberg (FAU), Erlangen, Germany.
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$a Christiansen, Silke $u Max Planck Institute for the Science of Light, Erlangen, Germany. Helmholtz-Zentrum Berlin für Materialien und Energie, Berlin, Germany. Physics Department, Freie Universität Berlin, Berlin, Germany.
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$a Herrmann, Martin $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Bozec, Aline $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Gruber, Robert $u Department of Dermatology, Venereology, and Allergology, Medical University of Innsbruck, Innsbruck, Austria.
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$a Schett, Georg $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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$a Hoffmann, Markus H $u Department of Medicine 3, Friedrich Alexander University of Erlangen-Nürnberg, Universitätsklinikum Erlangen, Erlangen, Germany.
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