-
Views
-
Cite
Cite
Clément Cochain, Hafid Ait-Oufella, Alma Zernecke, Neutrophils promote atherosclerotic plaque destabilization in a mouse model of endotoxinaemia, Cardiovascular Research, Volume 114, Issue 12, 01 October 2018, Pages 1573–1574, https://doi.org/10.1093/cvr/cvy168
Close - Share Icon Share
Extract
This editorial refers to ‘Neutrophils recruited by leukotriene B4 induce features of plaque destabilization during endotoxaemia’ by M.-A. Mawhin et al., pp. 1656–1666.
Atherosclerosis is regarded as a chronic inflammatory disease involving both innate and adaptive immunity. Besides their critical team leader role in acute infections, neutrophils can also be found at low numbers in murine atherosclerotic lesions as well as in human coronary and carotid artery plaques.1,2 In the past decade, multiple pathogenic roles of neutrophils have emerged at various stages of atherosclerosis.1 For instance, neutrophil depletion using anti-Ly6G antibodies reduces early atherogenesis, suggesting a role in lesion initiation.1 Neutrophils may also promote vascular inflammation via neutrophil extracellular trap (NET)-mediated priming of pro-inflammatory macrophages activity3 and the proteolytic activation of cytokines.1 In addition, neutrophils are considered to promote plaque-erosion and atherothrombosis.4,5 Despite all these recent advances in our understanding of neutrophil biology in both atherosclerosis development and complications, the mechanisms mediating neutrophil recruitment and their role in atherosclerosis are still far from being fully elucidated.
