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      Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury

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          Abstract

          Neutrophils, the most abundant human immune cells, are rapidly recruited to sites of infection, where they fulfill their life-saving antimicrobial functions. While traditionally regarded as short-lived phagocytes, recent findings on long-term survival, neutrophil extracellular trap (NET) formation, heterogeneity and plasticity, suppressive functions, and tissue injury have expanded our understanding of their diverse role in infection and inflammation. This review summarises our current understanding of neutrophils in host-pathogen interactions and disease involvement, illustrating the versatility and plasticity of the neutrophil, moving between host defence, immune modulation, and tissue damage.

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          Netting neutrophils in autoimmune small-vessel vasculitis.

          Kai Kessenbrock, Markus Krumbholz, Ulf Schönermarck … (2009)
          Small-vessel vasculitis (SVV) is a chronic autoinflammatory condition linked to antineutrophil cytoplasm autoantibodies (ANCAs). Here we show that chromatin fibers, so-called neutrophil extracellular traps (NETs), are released by ANCA-stimulated neutrophils and contain the targeted autoantigens proteinase-3 (PR3) and myeloperoxidase (MPO). Deposition of NETs in inflamed kidneys and circulating MPO-DNA complexes suggest that NET formation triggers vasculitis and promotes the autoimmune response against neutrophil components in individuals with SVV.
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            Dynamic NETosis is Carried Out by Live Neutrophils in Human and Mouse Bacterial Abscesses and During Severe Gram-Positive Infection

            Bryan G Yipp, Björn Petri, Davide Salina … (2012)
            Neutrophil extracellular traps (NETs) are released, as neutrophils die in vitro, in a process requiring hours, leaving a temporal gap for invasive microbes to exploit. Functional neutrophils undergoing NETosis have not been documented. During Gram-positive skin infections, we directly visualized live PMN in vivo rapidly releasing NETs, which prevented bacterial dissemination. NETosis occurred during crawling thereby casting large areas of NETs. NET-releasing PMN developed diffuse decondensed nuclei ultimately becoming devoid of DNA. Cells with abnormal nuclei displayed unusual crawling behavior highlighted by erratic pseudopods and hyperpolarization consistent with the nucleus being a fulcrum for crawling. A combined requirement of Tlr2 and complement mediated opsonization tightly regulated NET release. Additionally live human PMN developed decondensed nuclei and formed NETS in vivo and intact anuclear neutrophils were abundant in Gram-positive human abscesses. Therefore early in infection, non-cell death NETosis occurs in vivo during Gram-positive infection in mice and humans.
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              A novel mechanism of rapid nuclear neutrophil extracellular trap formation in response to Staphylococcus aureus.

              Florian Pilsczek, Davide Salina, Karen K. H. Poon … (2010)
              Neutrophil extracellular traps (NETs) are webs of DNA covered with antimicrobial molecules that constitute a newly described killing mechanism in innate immune defense. Previous publications reported that NETs take up to 3-4 h to form via an oxidant-dependent event that requires lytic death of neutrophils. In this study, we describe neutrophils responding uniquely to Staphylococcus aureus via a novel process of NET formation that did not require neutrophil lysis or even breach of the plasma membrane. The multilobular nucleus rapidly became rounded and condensed. During this process, we observed the separation of the inner and outer nuclear membranes and budding of vesicles, and the separated membranes and vesicles were filled with nuclear DNA. The vesicles were extruded intact into the extracellular space where they ruptured, and the chromatin was released. This entire process occurred via a unique, very rapid (5-60 min), oxidant-independent mechanism. Mitochondrial DNA constituted very little if any of these NETs. They did have a limited amount of proteolytic activity and were able to kill S. aureus. With time, the nuclear envelope ruptured, and DNA filled the cytoplasm presumably for later lytic NET production, but this was distinct from the vesicular release mechanism. Panton-Valentine leukocidin, autolysin, and a lipase were identified in supernatants with NET-inducing activity, but Panton-Valentine leukocidin was the dominant NET inducer. We describe a new mechanism of NET release that is very rapid and contributes to trapping and killing of S. aureus.
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                Author and article information

                Contributors
                Christoph Dehio: Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS Pathog
                Journal ID (iso-abbrev): PLoS Pathog
                Journal ID (publisher-id): plos
                Journal ID (pmc): plospath
                Title: PLoS Pathogens
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Print): 1553-7366
                ISSN (Electronic): 1553-7374
                Publication date (Electronic): 12 March 2015
                Publication date Collection: March 2015
                Volume: 11
                Issue: 3
                Electronic Location Identifier: e1004651
                Affiliations
                [1 ]Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
                [2 ]Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Mainz, Germany
                [3 ]Institute of Cell Biology, Department of Immunology, University of Tübingen, Tübingen, Germany
                [4 ]Department of Pediatrics I, University of Tübingen, Tübingen, Germany
                [5 ]3rd Dept. of Medicine, Johannes Gutenberg-University Medical Center, Mainz, Germany
                [6 ]Department of Pediatric Pneumology and Immunology, Charité Hospital, Humboldt University, Berlin, Germany
                [7 ]Fachbereich Immunologie, Labor Berlin Charité Vivantes GmbH, Berlin, Germany
                [8 ]Theodor Kocher Institute, University of Bern, Bern, Switzerland
                [9 ]Sanquin Research and Landsteiner Laboratory, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
                [10 ]Department of Internal Medicine II, University of Tübingen, Tübingen, Germany
                University of Basel, SWITZERLAND
                Author notes

                The authors have declared that no competing interests exist.

                Article
                Publisher ID: PPATHOGENS-D-14-02099
                DOI: 10.1371/journal.ppat.1004651
                PMC ID: 4357453
                PubMed ID: 25764063
                SO-VID: baf6fb26-efb1-48ee-b803-0506bc945f66
                Copyright statement: Copyright @ 2015
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

                History
                Page count
                Figures: 1, Tables: 0, Pages: 22
                Funding
                This work was supported by the German Research Foundation (DFG, Emmy Noether Programme HA 5274/3-1 to DH) and the CRC/SFB685 at Tübingen. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Review

                ScienceOpen disciplines: Infectious disease & Microbiology
                Data availability:
                ScienceOpen disciplines: Infectious disease & Microbiology

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