Modulating local dermal inflammatory response improves survival in a post-burn pneumonia model

Abstract

Objective: Infectious complications following burn injury, such as pneumonia, are associated with a significant increase in morbidity and mortality. We previously demonstrated that post-burn modulation of dermal inflammatory signaling effectively attenuated systemic inflammatory response and burn-induced lung injury. Dermal inflammation was reduced by application of a topical inhibitor of p38 MAPK, a pivotal stress signaling pathway, to the burned skin. We now hypothesize that post-burn inhibition of dermal inflammatory signaling will improve survival in a second-hit pneumonia model.