Intravascular Danger Signals Guide Neutrophils to Sites of Sterile Inflammation

By B. McDonald, K. Pittman, G. Menezes, S. Hirota, I. Slaba, C. Waterhouse, P. Beck, D. Muruve, P. Kubes. Science, 2010

1,195 citations recorded by the source corpus.

Subfields: Immunology, Neurology

View Paper: https://www.semanticscholar.org/paper/706855260653b4e12f9ee48a89381bf90801d4f6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. A. Mantovani
2. P. Kubes
3. G. Shadel
4. S. Jaillon
5. J. Zindel
6. A. West
7. S. Ghosh
8. Caroline L. Sokol

In Neurology

1. A. Mantovani
2. J. Zindel
3. W. Junger
4. P. Kubes

Citations in the corpus

• Liver inflammation and fibrosis. (2017, background): “org Volume 127 Number 1 January 2017 injury area (25).”
• Neutrophils: Between Host Defence, Immune Modulation, and Tissue Injury (2015, background): “Neutrophil infiltration is not limited to infectious conditions and also occurs in sterile environments, mediated by a multistep migratory sequence, involving the inflammasome, chemokines, and formyl-peptide signals [175].”
• Platelets release mitochondria serving as substrate for bactericidal group IIA-secreted phospholipase A2 to promote inflammation. (2014, background): “Similar to bacteria, mitochondria express N-formylated peptides that can recruit leukocytes to the site(s) of inflammation.(12,57) The presence of these different inflammatory components, whose production does not require sPLA2-IIA, may explain how intravenous injection of mitochondria induce neutro”
• Ischemia/Reperfusion (2016, positive): “the NLRP3 inflammasome, which in turn functions to induce neutrophil infiltration into ischemic tissues (548, 764).”
• Immune cell regulation by autocrine purinergic signalling (2011, background): “Such interconnected mechanisms, including ATP release, inflammasome activation, IL-8 secretion and FPR-mediated chemotaxis, were recently shown to regulate recruitment of neutrophils to sites of inflammatio”
• Chemokines and chemokine receptors: positioning cells for host defense and immunity. (2014, background): “These mitochondrial formyl peptides bind to the formyl peptide receptor 1 (FPR1) and promote neutrophil chemotaxis to the site of cellular injury (94, 95).”
• DAMPs, PAMPs, and LAMPs in Immunity and Sterile Inflammation. (2020, background): “Although their canonical role is to battle microbes, a growing body of evidence suggests that they are imperative for timely restoration of tissue architecture in sterile injury (10, 68).”
• Cell Biology of Ischemia/Reperfusion Injury (2012, background): “…of an appropriate site for neutrophil infiltration may be a gradient of chemoattractant signals arising from damaged and dying cells which serve as a guide to allow intravascular homing of the leukocyte strictly to foci of injury before they are allowed to diapedese (McDonald et al., 2010).”
• The chemokine system in innate immunity. (2015, background): “Instead, endogenous formyl peptides, which are produced by mitochondria and released upon cellular damage, promoted neutrophil chemotaxis to the site of cellular injury (McDonald et al. 2010; Zhang et al. 2010).”
• Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME (2013, positive): “The signals triggering their recruitment are also present in sterile inflammation such as tissue injury by chemicals or trauma (McDonald et al. 2010; Rock et al. 2011).”