Neutrophil extracellular traps (NETs), which consist of neutrophil DNA and cytoplasmic proteins, have been shown to be involved in various infectious, inflammatory, and autoimmune diseases. Neutrophil extracellular traps are abundant at the site of infection and acute inflammation. Neutrophil extracellular trap formation can occur through various intracellular signaling pathways, including peptidylarginine deiminase 4, Raf-MEK-ERK, nitric oxide, Toll-like receptor 4, high mobility group box 1, pentraxin 3, and mammalian targets of rapamycin. A growing body of evidence indicates that NETs may play an important role in injury, and decreases in NETs could reduce tissue injury. Neutrophil extracellular traps are believed to modulate the inflammatory and immune responses of individuals after injury. In this review, the role of NETs in injury, including traumatic injury, ischemia-reperfusion–induced injury, and sepsis, as well as the potential markers and therapeutic targets of NET-related injury will be discussed.
*Department of Anesthesiology, Chang Gung Memorial Hospital; and †College of Medicine, Chang Gung University, Taoyuan; and ‡Department of Anesthesiology, National Taiwan University Hospital, Taipei, Taiwan
Received 28 Nov 2013; first review completed 17 Dec 2013; accepted in final form 22 Jan 2014
Address reprint requests to Huang-Ping Yu, MD, PhD, Department of Anesthesiology, Chang Gung Memorial Hospital, 5 Fu-Shin St, Kwei-Shan, Tao-Yuan, Taiwan 333. E-mail: email@example.com.
This work was partially supported by grants from the National Science Council (NSC102-2314-B-182A-051-MY3) and Chang Gung Memorial Hospital (CMRPG3B1052) to H.-P.Y. Support was also provided by the National Science Council (NSC101-2314-B-182-082) and Chang Gung Memorial Hospital (CMRPG3B1622) to F.-C.L.