Abstract
Thermal injury results in changes in the inflammatory and innate immune response of pediatric patients. Plasma cytokines, cellular profiles, and reduction in innate immune function following burn injury have also been correlated to adverse outcomes (e.g., mortality and infectious complications). Changes in adaptive immune function following thermal injury are not as well characterized. Our goal was to better understand if adaptive immune dysfunction occurs early after pediatric thermal injury and is a risk factor for nosocomial infections (NIs). A prospective, longitudinal immune function observational study was performed at a single American Burn Association (ABA)-verified pediatric burn center. Eighty burn patients were enrolled with 20 developing NI, defined using Centers for Disease Control and Prevention (CDC) criteria. We collected whole blood samples from pediatric burn patients within the first 72 hours from injury and between days 4 and 7, where applicable to analyze adaptive immune function. We compared immune function between burn patients who went on to develop NI and those that did not. Within the first 72 hours of injury, burn patients who developed NI had significantly lower absolute CD4(+) lymphocyte counts and whole blood ex vivo phytohemagglutinin (PHA)-induced interferon gamma (IFN gamma) and interleukin-10 (IL-10) production capacity compared to those that did not develop infection. Further analysis using receiver operating characteristic curve revealed that PHA-induced IL-10 production capacity had the highest area under the curve. Our data demonstrate that early adaptive immune suppression occurs following pediatric thermal injury and PHA-induced IL-10 production capacity appears to be a predictor for the development of NI.
