Trauma remains the leading cause of years of life lost in the United States. Severe injuries involving hemorrhagic shock, fractures and other blunt or penetrating soft tissue destruction, can continue to threaten survival even after initial stabilization of the patient.
Our current rubric for this threat is that the initial insult releases mediators from hypoperfused gut and wound sites, predisposing distant organs to injury by way of priming circulating effector cells. Specifically, circulating mediators reprogram target leukocytes (and endothelium) to offer exaggerated responses (either as adaptive or, more commonly, in a maladaptive, pro-inflammatory, feed-forward loop).
Thus, our perpetual Center title ‘Trauma primes cells”, circa 1993, is a koan that i) recognizes different mediators and effector cells, and ii) reminds us that temporally staggered signaling permits early mediators to influence subsequent responses to resuscitation, transfusion, or infection.
In the 10 years since our initial funding we and other investigators have vied to identify the mediators, learn their signaling mechanisms, and design rational interventions. Based on this accumulated, albeit rudimentary, knowledge we retain the past cycle’s Center title ‘Therapy for Trauma primes Cells’.