Abstract
Burn injuries elicit a unique and dynamic stress response which can lead to burn injury progression. Though neutrophils represent crucial players in the burn-induced immunological events, the dynamic secretion pattern and systemic levels of neutrophil-derived factors have not been investigated in detail so far. Serum levels of neutrophil elastase (NE), myeloperoxidase (MPO), citrullinated histone H3 (CitH3), and complement factor C3a were quantified in burn victims over 4 weeks post injury. Furthermore, the potential association with mortality, degree of burn injury, and inhalation trauma was evaluated. In addition, leukocyte, platelet, neutrophil, and lymphocyte counts were assessed. Lastly, we analyzed the association of neutrophil-derived factors with clinical severity scoring systems. Serum levels of NE, MPO, CitH3, and C3a were remarkably elevated in burn victims compared to healthy controls. Leukocyte and neutrophil counts were significantly increased on admission day and day 1, while relative lymphocytes were decreased in the first 7 days post burn trauma. Though neutrophil-derived factors did not predict mortality, patients suffering from 3rd degree burn injuries displayed increased CitH3 and NE levels. Accordingly, CitH3 and NE were elevated in cases with higher abbreviated burn severity indices (ABSI). Taken together, our data suggest a role for neutrophil activation and NETosis in burn injuries and burn injury progression. Targeting exacerbated neutrophil activation might represent a new therapeutic option for severe cases of burn injury.
Highlights
Cause, inhalation injury, patient age, and chronic medical conditions9. Neutrophils[10] and macrophages[11] are early key players infiltrating the burn-injured area
We found that NETosis-associated factors were significantly increased compared to healthy controls (Fig. 1)
These data suggest a role for NETosis in the systemic post burn injury immune response
Summary
Cause, inhalation injury, patient age, and chronic medical conditions9. Neutrophils[10] and macrophages[11] are early key players infiltrating the burn-injured area. Neutrophils[10] and macrophages[11] are early key players infiltrating the burn-injured area Though these immune cells are readily activated by burn injury-induced damage-associated molecular patterns (DAMPs), macrophage antigen presentation and neutrophil-mediated killing of pathogens have been shown to be diminished following burn injury[12,13], leading to increased susceptibility to infections. Though secondary burn progression substantially promotes tissue damage, its role in the post injury tissue response is often underestimated. Activated protein-arginine deiminase 4 (PAD4) catalyzes citrullination of histones, which results in chromatin decondensation Granule proteins, such as myeloperoxidase (MPO) and neutrophil elastase (NE), further promote DNA de-compaction and intracellular DNA together with granule proteins are released following plasma membrane rupture[18,19]. We aimed to delineate the dynamics of neutrophil-derived immunomodulators to deepen our understanding of NETosis in the post-burn injury immune response
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