Rationale
Bacteremic trauma victims have a higher risk of death than their non-bacteremic counterparts. The role that altered immunity plays in the development of bacteremia is unknown.
Objective
Using an existing dataset, we sought to determine if differences in early post-injury immune-related gene expression are associated with subsequent gram-negative bacteremia (GNB).
Design
Retrospective cohort study, a secondary analysis of the Glue Grant database.
Subjects
Severely injured blunt trauma patients.
Setting
Seven level one trauma centers across the United States.
Measurements
Total leukocyte gene expression was compared between the subjects that developed GNB and those that did not.
Main Results
We observed that GNB was an independent risk factor for death (OR, 1.86; P=0.015). We then compared gene expression at 12 and 96 hours after injury in ten subjects who subsequently developed GNB matched to 26 that did not. At 12 hours, expression of 64 probes differed ≥1.5-fold; none represented genes related to innate or adaptive immunity. By 96 hrs, 102 probes were differentially expressed with 20 representing 15 innate or adaptive immunity genes; including downregulation of IL1B and upregulation of IL1R2, reflecting suppression of innate immunity in GNB subjects. We also observed downregulation of adaptive immune genes in the GNB subjects.
Conclusions
By 96 hours after injury, there are differences in leukocyte gene expression associated with the development of GNB, reflecting suppression of both innate and adaptive immunity. GNB after trauma is, in part, consequence of host immunity failure and may not be completely preventable by standard infection-control techniques.