A Novel Mechanism of Rapid Nuclear Neutrophil Extracellular Trap Formation in Response to Staphylococcus aureus

By F. Pilsczek, D. Salina, Karen Poon, Candace Fahey, B. Yipp, C. Sibley, S. Robbins, Francis H. Y. Green, Michael G. Surette, M. Sugai and 4 more. Journal of Immunology, 2010

1,106 citations recorded by the source corpus.

Subfields: Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/b90054f3555645c5ccf2069925b92188b8820cba

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In Genetics

1. M. Egeblad
2. M. Radic
3. E. Nakasone
4. M. Kaplan
5. P. Kubes

In Immunology

1. P. Kubes
2. K. Martinod
3. D. Wagner
4. B. McDonald
5. B. Yipp
6. M. Egeblad
7. M. Radic
8. E. Nakasone

Citations in the corpus

• Cancer cells induce metastasis-supporting neutrophil extracellular DNA traps (2016, background): “Of more than 50 evaluated neutrophils, none showed evidence of DNA-containing vesicles budding from the nucleus, which is the morphology described as typical for nonlytic NET-forming neutrophils (26).”
• NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis (2013, background): “NET formation may also occur through a rapid (10 min to 1 hour) nonlytic process independent of oxidant production (24).”
• Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “However, other studies suggested that ROS involvement depends on the stimulus [60–63].”
• A Myeloperoxidase-Containing Complex Regulates Neutrophil Elastase Release and Actin Dynamics during NETosis (2014, neutral): “A fraction of neutrophils have also been reported to release NETs without dying, leaving behind cytoplasts that continue to ingest microbes (Pilsczek et al., 2010; Yipp et al., 2012).”
• Biofilm formation in Staphylococcus implant infections. A review of molecular mechanisms and implications for biofilm-resistant materials. (2012, background): “Several staphylococcal components, like Panton-Valentine leukocidin, autolysin, and a lipase, display a NET-inducing activity, but Panton-Valentine leukocidin seems the dominant NET-inducer [137].”
• NETosis: how vital is it? (2013, methodology): “Here we describe at least 2 different mechanisms by which NETs are formed, including a suicide lytic NETosis and a live cell or vital NETosis.”
• The neutrophil in vascular inflammation (2011, background): “In higher order species, these functions have diverged into more specialized cells, but the platelet has retained some essential immune functions, particularly in partnership with neurophils 86, 87 .”
• Neutrophil Extracellular Traps and Its Implications in Inflammation: An Overview (2017, background): “Suicidal NETosis, with a duration of 2–4 h, is the best described model (14), even though its molecular processes are not fully understood (15).”
• Thrombosis: tangled up in NETs. (2014, background): “Here, the neutrophils rapidly expelNETs (withinminutes) in response to live Staphylococcus aureus.(19,20) The neutrophil ejects either a portion or all of its decondensed nuclear contents (Figure 1B) without releasing the cytoplasmic contents or lysing the plasma membrane.”
• SK3 channel and mitochondrial ROS mediate NADPH oxidase-independent NETosis induced by calcium influx (2015, methodology): “The plate reader assay is routinely used for monitoring NET DNA release (4, 6, 17), and it detects extracellular NETs with a cell impermeable, extracellular DNA dye Sytox Green.”
• Neutrophil extracellular traps (NETs): Double-edged swords of innate immunity (2012, background): “Notable examples of bacteria that potently induce NETs include Staphylococcus aureus (36, 37), Streptococcus sp.”
• Neutrophil extracellular traps sequester circulating tumor cells and promote metastasis. (2013, positive): “They have been observed to trap pathogens in vitro and in vivo (44, 46, 48).”