Platelet TLR4 activates neutrophil extracellular traps to ensnare bacteria in septic blood

By Stephen R. Clark, Adrienne C. Ma, Samantha A. Tavener, B. McDonald, Z. Goodarzi, M. Kelly, K. Patel, S. Chakrabarti, Erin F. McAvoy, G. Sinclair and 6 more. Nature Medicine, 2007

2,318 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Immunology

View Paper: https://www.semanticscholar.org/paper/1db26ef7b2a08b45458d9d0a596d40065265f3c8

How researchers see this paper

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In Epidemiology

1. P. Kubes
2. B. Yipp
3. C. Rosales
4. A. Mantovani
5. V. Papayannopoulos
6. Arturo Zychlinsky
7. Kathleen D. Metzler

In Genetics

1. Arturo Zychlinsky
2. V. Brinkmann
3. P. Kubes
4. C. Rosales
5. Michael G. Surette
6. C. Jenne
7. C. Goosmann
8. N. Mackman

In Immunology

1. P. Kubes
2. Arturo Zychlinsky
3. V. Brinkmann
4. V. Papayannopoulos
5. C. Rosales
6. K. Martinod
7. D. Wagner
8. B. Yipp

Citations in the corpus

• Intravascular neutrophil extracellular traps capture bacteria from the bloodstream during sepsis. (2012, methodology): “during E. coli-Induced Sepsis NETs have been implicated in immune-mediated tissue damage in a number of diseases including endotoxemia (Clark et al., 2007; Papayannopoulos and Zychlinsky, 2009).”
• Platelets and the immune continuum (2011, neutral): “Trapping was dependent on TLR4 + platelets binding LPS and adhering to neutrophils, resulting in neutrophil activatio”
• Neutrophil Extracellular Traps Contain Calprotectin, a Cytosolic Protein Complex Involved in Host Defense against Candida albicans (2009, background): “Neutrophils of several species make NETs [7,8,9] and they might be important in the immune defense against bacteria and fungi [10,11,12,13].”
• Neutrophil extracellular traps (NETs): Double-edged swords of innate immunity (2012, background): “Platelet–neutrophil interactions leading to NETs may play important roles in ECs and tissue damage not only during sepsis, but also in chronic inflammatory disorders (22).”
• Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo (2012, background): “Although release of NETs has been previously observed in a baboon model of venous thrombosis and in sepsis-induced microcirculatory thrombosis (Clark et al., 2007; Fuchs et al., 2010), the functional consequences of NETosis and their in vivo relevance for thrombogenesis in large veins remain…”
• Cancers predispose neutrophils to release extracellular DNA traps that contribute to cancer-associated thrombosis (2012, background): “Given the close interaction of platelets and neutrophils during infection and the implication of platelet activation in the generation of NETs (39, 40), their potential contribution in the cancer models should be addressed.”