Neutrophil Extracellular Traps Kill Bacteria
Abstract
Neutrophils engulf and kill bacteria when their antimicrobial granules fuse with the phagosome. Here, we describe that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria. These neutrophil extracellular traps (NETs) degrade virulence factors and kill bacteria. NETs are abundant in vivo in experimental dysentery and spontaneous human appendicitis, two examples of acute inflammation. NETs appear to be a form of innate response that binds microorganisms, prevents them from spreading, and ensures a high local concentration of antimicrobial agents to degrade virulence factors and kill bacteria.
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The role of these nucleases has been ascribed not to altering the bacteria's own extracellular DNA but to disrupting neutrophil extracellular traps.
“Interestingly, the role of these nucleases has been ascribed not to altering the bacteria’s own extracellular DNA but to disrupting neutrophil extracellular traps.171”
From The dental plaque biofilm matrix (2021) · cites this paper as [171]
A network of granule proteins and DNA, the neutrophil extracellular trap (NET), is formed to immobilize bacteria, degrade virulence factors, and allow neutrophils to phagocytize pathogens.
“A network of granule proteins and DNA (in particular chromatin) is also formed, referred to as the neutrophil extracellular trap (NET), which is actively made to immobilize bacteria, degrade virulence factors, and allow neutrophils to phagocytize pathogens.[ 54 ]”
From Unraveling and Harnessing the Immune Response at the Cell–Biomaterial Interface for Tissue Engineering Purposes (2024) · cites this paper as [54]
Neutrophils can eliminate organisms residing in the extracellular environment through the deployment of neutrophil extracellular traps (NETs).
“More recent evidence indicates that neutrophils can also eliminate organisms residing in the extracellular environment through the deployment of neutrophil extracellular traps (NETs).”
From Immunology of Wound Healing (2018) · cites this paper as [42]
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- Authors
- Brinkmann, V., Reichard, U., Goosmann, C., Fauler, B., Uhlemann, Y., Weiss, D. S., Weinrauch, Y., & Zychlinsky, A.
- Affiliations
- Max Planck Institute for Infection Biology (DE)
- Corresponding author
- Zychlinsky, Arturo
- Venue
- Science
- Published
- 2004-03-05
- Volume
- 303
- Issue
- 5663
- Pages
- 1532-1535
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2104934425
- Cited by
- 10,268
- References
- 15
- Citations by year
- 2026: 705 · 2025: 802 · 2024: 860 · 2023: 868 · 2022: 891 · 2021: 909 · 2020: 795 · 2019: 663 · 2018: 573 · 2017: 539 · 2016: 529 · 2015: 416 · 2014: 398 · 2013: 324 · 2012: 290
- FWCI
- 20.02
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI037720, AI037720)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Life Sciences › Immunology and Microbiology › Microbiology › Antimicrobial Peptides and Activities
- Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
- Keywords
- neutrophil extracellular traps, neutrophils, bacterial killing, chromatin, Gram-positive bacteria, Gram-negative bacteria, dysentery, appendicitis, innate immunity, acute inflammation, phagosome
- MeSH terms
- Animals, Appendicitis, Bacterial Proteins, Blood Bactericidal Activity, Cytoplasmic Granules, DNA, Dysentery, Bacillary, Histones, Humans, Immunity, Innate, Microscopy, Electron, Neutrophils, Endopeptidases, Phagocytosis, Rabbits, Salmonella typhimurium, Shigella flexneri, Staphylococcus aureus, Cytochalasin D, Neutrophil Activation, Leukocyte Elastase, Virulence Factors
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