Trauma is the fifth leading cause of death in the United States. Patients over 65 years of age represent a disproportionally large percentage of those individuals and are at a significantly greater risk of morbid outcomes following such injuries. In this regard, we have previously demonstrated that in geriatric patients, unlike young patients, the mere presence of a systemic inflammatory response syndrome (SIRS), not the degree of SIRS, is predictive of death, suggesting a differential impact of SIRS upon geriatric versus young patients. We have also shown considerable differences in trauma care management in geriatric patients, including head injury, suicides, and tracheotomy care, and urinary tract infections. It is essential to understand the inflammatory profile, and specifically the lymphocyte component, of geriatric patients and how they differ from young patients. We postulate that geriatric trauma victims will display an overall altered inflammatory response in both the pro and anti-inflammatory cytokines as well as a greater degree of lymphocyte energy compared with younger trauma patients. Understanding how geriatric trauma patients differ in respect to their inflammatory and lymphocyte response to trauma will help direct interventions aimed at improving survival for this vulnerable population.
Sepsis, a commonly encountered morbid outcome of significant trauma, contributes substantially to healthcare costs, morbidity, and mortality among critically ill surgical patients. The implementation of new modalities in critical care, including early goal-directed fluid therapy and antimicrobial regimens, has failed to ameliorate these significant problems. Our studies seek to determine how invariant natural killer T-cells (iNKT-cells) participate in and influence other elements of the coordinated immune response to sepsis. To do this, we utilize the cecal ligation and puncture (CLP) model of polymicrobial sepsis to evaluate how sepsis induces changes in iNKT-cell structure and function, and how such changes alter other immune cells. We strongly believe that such knowledge will be critical not only to understanding the complex regulation of the immune system in response to infection, but also in identifying potential targets for the treatment of sepsis.