Abstract
After severe trauma, the resulting excessive inflammatory response is countered by compensatory anti-inflammatory mechanisms. The systemic inflammatory response to trauma enhanced by inappropriately timed surgical second hits may be detrimental for the patient. On the other hand, overwhelming anti-inflammatory mechanisms may put patients at increased risk from secondary local and systemic infections. The ensuing sepsis and organ dysfunction due to immune dysregulation remain the leading causes of death after injury. To date, there are no clinically applicable techniques to monitor the pro-/anti-inflammatory immune status of the patients and the remaining ability to react to microbial stimuli. Therefore, in the present study, we used a highly standardized and easy-to-use system to draw peripheral whole blood from polytraumatized patients (ISS≥32, n=7) and to challenge it with bacterial lipopolysaccharide. Secreted cytokines were compared with those in samples from healthy volunteers. We observed a significant decrease in the release of monocyte-derived mediators. Surprisingly, we detected stable or even increased concentrations of cytokines related to T cell maturation and function. For clinical practicability, we reduced the incubation time before supernatants were collected. Even after an abbreviated stimulation period, a stable release of almost all analysed parameters in patient blood could be detected. In conclusion, the data are indicative of a clinically well-applicable approach to monitor the immune status in severely injured patients in a short time. This may be used to optimize the timing of necessary surgical interventions to avoid a boost of proinflammation and reduce risk of secondary infections.
Highlights
This study was performed with two aims: (a) to define the alterations in immune reaction to a defined microbial stimulus after severe trauma, and (b) to test the applicability of a standardized whole blood model for clinical monitoring of the immune function
We were able to confirm that pro‐inflammatory cytokines predominantly secreted by monocytes and macrophages, and by lymphocytes, are reduced when whole blood is challenged with a pathogen‐associated molecular pattern early after severe trauma.[3,4,9,16,17,18]
It was surprising that 24 hours after injury, the TNF response was not as profoundly impaired as at the other time points
Summary
Severe injury and the subsequent development of a systemic inflammatory response syndrome (SIRS) and sepsis often lead to multiple organ dysfunction and failure, resulting in a substantial morbidity in trauma victims.[1,2,3,4,5] It is a long‐known paradox that excessive immune activation due to vast amounts of endogenous cellular components released after massive tissue trauma and exogenous pathogen‐derived danger molecules can be associated with a compensatory anti‐inflammatory response which may render the patient susceptible to infections.[6,7,8,9]. The present study was performed to find out whether (a) a whole blood ex vivo system can be used to monitor the pro‐ and anti‐inflammatory immune responsiveness of trauma patients, and (b) whether a 24 hours standard incubation time of this ex vivo system can be reduced to a 4 hours incubation period without loss of discriminatory power
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