Abstract
BackgroundFollowing tissue injury after trauma, the activation of innate immune pathways results in systemic inflammation, organ failure and an increased risk of infections. The objective of this study was to characterize the kinetics of the S100A8/S100A9 complex, a new-recognized alarmin, as well as its soluble receptor sRAGE, over time after trauma as potential early biomarkers of the risk of organ damage.MethodsWe collected comprehensive data from consenting patients admitted to an ICU following severe trauma. The blood samples were taken at Day 0 (admission), Day1, 3 and 5 S100A8/A9 and sRAGE were measured by ELISA. Biomarkers levels were reported as median (IQR).ResultsThirty-eight patients sustaining in majority a blunt trauma (89%) with a median ISS of 39 were included. In this cohort, the S100A8/A9 complex increased significantly over time (p = 0.001), but its levels increment over time (D0 to D5) was significantly smaller in patients developing infection (7.6 vs 40.1 mcg/mL, p = 0.011). The circulating level of sRAGE circulating levels decreased over time (p < 0.0001) and was higher in patients who remained in shock on day 3 (550 vs 918 pg/mL; p = 0.02) or 5 (498 vs 644 pg/mL; p = 0.045). Admission sRAGE levels were significantly higher in non-survivors (1694 vs 745 pg/mL; p = 0.015) and was higher in patients developing renal failure (1143 vs 696 pg/mL, p = 0.011).DiscussionOur findings reveal an interesting association between the biomarker S100A8/9 least increase over time and the presence of infectious complication after trauma. We describe that the sRAGE decline over time is in relation with shock and markers of ischemic injury. We also confirm the association of sRAGE levels measured at admission with mortality and the development of renal failure.ConclusionsThis work illustrates the importance of following the circulating level of biomarker overtime. The utilization of S1008/9 as a tool to stratify infection risk and trigger early interventions need to be validated prospectively.
Highlights
Following tissue injury after trauma, the activation of innate immune pathways results in systemic inflammation, organ failure and an increased risk of infections
Traumatic injury is the leading global cause of mortality for individuals between 15 and 44 years of age [1, 2]. Patients surviving their initial resuscitation following severe trauma are at risk of subsequent complications such as sepsis and multiple organ dysfunction syndrome (MOD), which are responsible for late morbidity and mortality [3,4,5]
Blood samples were available for analysis in 38 (100%) patients on day 0, in 36 (95%) on day 1, in 33 (87%) on day 3, and in all four sampling time points for 30 (79%) of the enrolled subjects
Summary
Following tissue injury after trauma, the activation of innate immune pathways results in systemic inflammation, organ failure and an increased risk of infections. Traumatic injury is the leading global cause of mortality for individuals between 15 and 44 years of age [1, 2] Patients surviving their initial resuscitation following severe trauma are at risk of subsequent complications such as sepsis and multiple organ dysfunction syndrome (MOD), which are responsible for late morbidity and mortality [3,4,5]. Tissue injury secondary to trauma results in the release of endogenous molecules, that have been called damage-associated molecular patterns (DAMPs). These endogenous molecules, known as alarmins, are released passively from necrotic cells, or actively by alternative secretion pathways, and contribute to tissue damage [6, 7]. They bind to several receptors, including the receptor for advanced glycation endproducts (RAGE), Toll-like receptor 4, and the formyl peptide receptors [9]
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