Tranexamic Acid Suppresses the Release of Mitochondrial Damps and Reduces Lung Inflammation in a Murine Burn Model

Introduction Severe burn injuries are known to initiate a profound systemic inflammatory response (SIRS) that may lead to burn shock and other SIRS related complications. Damage associated molecular patterns (DAMPs) are important early signaling molecules that initiate SIRS after burn injury. Mitochondrial DAMPs (mtDAMPs) – such as mitochondrial DNA (mtDNA) - are thought to be the most critical of these early signaling molecules. Previous work in a rodent model has shown that application of a topical immune modulator (p38 MAPK inhibitor) applied directly to the burn wound decreases cytokine expression, reduces pulmonary inflammation and edema and improves survival. Our group has demonstrated that tranexamic acid (TXA) – in addition to its use as an anti-fibrinolytic – has cell protective in vitro effects. We hypothesized that administration of TXA after burn injury would attenuate mtDAMP release and reduce lung inflammation.