(Accessed 15 July 2017)
Time for trauma immunology
Timothy R. Billiar, Yoram Vodovotz
| published 11 Jul 2017 PLOS Medicine
While it is intuitive that the damage to bones and soft tissues causes both short- and long-term “organic” dysfunction, the “illness” caused by injury is less appreciated. This results from the systemic manifestations that follow the physiologic, immunologic, and metabolic changes induced by shock from blood loss and direct tissue destruction. The immunologic changes following injury are profound, and have been measured in the circulating leukocytes of injured humans as a massive activation of the innate immune system and a near-simultaneous impairment in adaptive immune responses . This “immune dysfunction,” seen after even moderate injury, can be appreciated clinically as inflammation-associated organ dysfunction (typically peaking on day 2 to day 3 postinjury) and a sustained increase in the susceptibility to secondary infections, especially pneumonia [1,2]. The 2 processes are thought to be linked by the proximal events that activate the immune system immediately following a traumatic event.