**1. Introduction**

Despite recent improvements in the care of the injured, severe trauma remains a major bur‐ den on our society, resulting in the annual death of more than five million people world‐ wide (World Health Organisation. Injuries and violence: the facts. 2014. http://www.who.

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int/violence\_injury\_prevention/key\_facts/en/ Accessed 9 May 2016). Tissue injury, traumatic shock and subsequent resuscitation and surgical interventions lead to localised and systemic inflammatory responses. Polymorphonuclear (neutrophil) granulocytes (PMNs) are an essen‐ tial part of the innate immune responses and key instigators and effectors of the underlying pathological mechanisms (endothelial damage, interstitial histolysis, cytokine production, phagocytosis) leading to post‐injury inflammation and secondary tissue injury. In 2004, the formation of neutrophil extracellular traps (NETs) was identified as an additional defence mechanism of PMN against microbes [1]. Since the initial description of their antibacterial function, a series of studies reported the existence of NETs in response to various types of sterile inflammations including traumatic injury [2–5]. The precise triggers, contributions and outcomes of NETs in trauma patients are not well understood. Given the significant clinical impact of sterile inflammation in these patients, understanding the role of NETosis may iden‐ tify novel biomarkers or therapeutic strategies to minimise post‐injury tissue damage and hyperinflammation. In this chapter, we summarise our current knowledge and existing gaps on post‐injury NET formation.
