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The host response to trauma and burns in the critically ill 

The host response to trauma and burns in the critically ill
Chapter:
The host response to trauma and burns in the critically ill
Author(s):

Edward A. Bittner

and Shawn P. Fagan

DOI:
10.1093/med/9780199600830.003.0304
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date: 29 November 2020

Following severe traumatic injury, patients enter a state of immune dysregulation consisting of both exaggerated inflammation and immune suppression. Traditionally, the host response has been viewed as an early systemic inflammatory response syndrome (SIRS) followed temporally by a compensatory anti-inflammatory or immune-suppressive response syndrome (CARS). While this paradigm has been widely accepted across both medical and scientific fields, recent advances have challenged this concept. The Glue grant investigators recently characterized both the initial inflammatory response to injury and the dynamic evolving recovery process. They found: (1) severe injury produces a rapid (< 12 hours) genomic reprioritization in which 80% of the leukocyte transcriptome is altered; (2) similarities in gene expression patterns between different injuries reveal an apparently fundamental response to severe inflammatory stress, which is far more common than different; (3) alterations in the expression of classical inflammatory and anti-inflammatory as well as adaptive immunity genes occur simultaneously, not sequentially after severe injury; (4) the temporal nature of the current SIRS/CARS paradigm is not supported at the level of the leukocyte transcriptome. Complications are not associated with genomic evidence of a ‘second hit’ and differ only in the magnitude and duration of this genomic reprioritization. Furthermore, the delayed clinical recovery with organ injury is not associated with dramatic qualitative differences in the leukocyte transcriptome. Finally, poor correlation between human and rodent inflammatory genomic responses will alter how the host response is studied in the future.

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