Dr. Jon Hazeldine
Research Fellow, University of Birmingham.
August 1, 2017 · 21 Reads

Prehospital immune response to major injury has been identified

Editor's note: By analysing blood samples obtained from traumatically-injured patients at the roadside, researchers at the University of Birmingham have described the changes that occur in the immune system within 1-hour of major injury. Studying the immediate immune response to injury may help identify patients at risk of poor clinical outcome, help in stratification for treatment and also aid in the development of novel therapies.

Motivation behind the research

Although the major and immediate cause of death following an accident is excessive bleeding, many victims later die following complications such as multi organ failure or infection. An individual’s immune response to injury significantly influences their chances of developing such life-threatening conditions as multiple organ dysfunction syndrome (MODS).

Multiple organ dysfunction syndrome (MODS) is a sequential derangement of individual organs; it is a process rather than a single event. It can lead to organ dysfunction or irreversible organ failure.

Previous research has suggested that analysing the immune system post-injury can identify patients at risk of poor outcome. However, almost all previous research that has examined the immune response to injury has analysed blood samples acquired from patients following their admission to hospital. Thus, the time from patient injury (e.g. road accident) to sample acquisition has ranged from hours to days post-trauma. Consequently, little is known regarding the status of the immune system in the immediate aftermath of injury and its relationship to patient outcome.

The Discovery

In collaboration with the West Midlands Air Ambulance Service (UK), blood samples were collected at the roadside from 89 critically-injured patients within 1-hour of injury. A comprehensive assessment of the immune system was performed in order to understand the changes that occur in the number and function of immune cells in the immediate aftermath of trauma.

Interestingly, we found evidence of simultaneous activation and suppression of the immune system within minutes of injury. Furthermore, we found within 1-hour of injury, patients who later developed multiple organ dysfunction syndrome (MODS) had significantly higher numbers of a specific immune cell, namely natural killer T cells, in their blood samples when compared to patients who did not develop MODS.

Natural killer T cells are known to play a crucial role in the response to infectious agents.

Study Limitations

The results of our study are based on the analysis of samples acquired from 89 patients. Our findings therefore require confirmation and validation in a larger independent set of patients.

The Future

Our study has provided a novel insight into the changes that occur in a patients immune system prior to their admission to hospital. If confirmed in subsequent independent studies, an assessment of blood samples collected within minutes of injury could help doctors identify patients at higher risk of poor outcome. Such information could support clinical decision making and patient management.

The complex nature of the acute immune response to injury suggests that targeting one element of the immune response is unlikely to reduce the incidence of multiple organ dysfunction syndrome (MODS). As we know what is being altered, our goal now is to try and understand the mechanisms behind these alterations.

Research article: Prehospital immune responses and development of multiple organ dysfunction syndrome following traumatic injury: A prospective cohort study. PLOS Medicine, 2017.

Scientists Bio: 
Dr Jon Hazeldine is a Research Fellow in the Institute of Inflammation and Ageing at the University of Birmingham, UK. In addition to science, Jon is an avid follower of West Bromwich Albion Football Club and a keen golf player. 
Professor Janet M Lord is the director of the MRC-ARUK Centre for Musculoskeletal Ageing Research and the Institute of Inflammation and Ageing at the University of Birmingham. This study was funded by NIHR SRMRC.

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