Modern Aspects of Burn Injury Immunopathogenesis and Prognostic Immunobiochemical Markers (Mini-Review)

Abstract

Burn injuries are among the most common peacetime injuries, with mortality ranging from 2.3% to 3.6%. At the same time, 85–90% of patients with burns are people of working age and children. Burn injury leads to metabolic disorders and systemic inflammatory response, inefficient energy consumption, and other physiological changes that can lead to dysfunction of organs and systems. The most formidable complication of burn injuries is sepsis mediated by multiple organ failure, the most common cause of poor prognosis in patients and has specific differences in these injuries. The purpose of this article was to dwell in detail on the most promising immunobiochemical markers of sepsis in the format of a mini-review, based on the main aspects of the immunopathogenesis of this complication. The pathogenesis of a burn injury and any general pathological process is based on an inflammatory reaction and large-scale changes in the skin and mucous membranes. This review is devoted to the progress in understanding the main aspects of the immunopathogenesis of burn lesions and the features of post-burn immune dysfunction, manifested by disorders in the innate and adaptive immunity systems. Attention is focused on the role in the immunopathogenesis of the development of systemic and local disorders in burn injury. Characterization of primary immunobiochemical markers of burn injury (cytokines, growth factors, C-reactive protein, procalcitonin, presepsin, matrix metalloproteinases, reactive oxygen species, nitric oxide, hemostasis parameters) is presented. The problem of treating burn lesions is associated with constant monitoring of the condition of patients and regular monitoring of specific immunobiochemical markers predicting sepsis for the timely initiation of a specific therapy.

Multiplexed Human Gene Expression Analysis Reveals a Central Role of the TLR/mTOR/PPARγ and NFkB Axes in Burn and Inhalation Injury-Induced Changes in Systemic Immunometabolism and Long-Term Patient Outcomes

“…Secondly, no patient clinical outcome prediction exists. Although it is evident that the immune dysfunction induced by burn injury correlates with short- and long-term patient outcomes, there is no practical model with a predictive value that accurately reflects the underlying degree of immune insult and significantly correlates with the degree of compromise [ 17 ]. In addition, although multi-center bio-informatic studies have described the genomic storm after injury and initial attempts have been made [ 4 , 30 , 31 ], a profile of immune gene expression from burn patients that can be transformed into an “immune suppression index” has not been translated to the clinic, nor have these genomic markers been used to inform clinical care.…”

“…Thus, it is plausible that the immune and metabolic system dysfunction resulting from DAMP-induced activation of the TLR/mTOR/PPARγ pathway is responsible for poor patient outcomes. Although previous studies have explored immunological dysfunction during burn injury, no study has identified biomarkers, which can inform the clinical decision-making to assess patients’ immune status, contributing to poor patient outcomes [ 17 ]. Here, an unbiased survey of immune and metabolic gene expression was performed within peripheral blood monocytic cells (PBMCs) obtained early after injury (<48 h) from burn patients, with and without inhalation injury.…”

An Overview of Recent Developments in the Management of Burn Injuries

“…Much progress has been made in understanding the immunopathogenesis of burns and disorders of innate and adaptive immunity. Immunobiochemical markers predictive of sepsis, such as cytokines, growth factors, C-reactive protein, procalcitonin, presepsin, matrix metalloproteinases, reactive oxygen species, nitric oxide and hemostasis parameters, should be monitored to allow the timely initiation of a specific therapy [465]. However, traditional indicators of sepsis show poor performance, mainly due to hypermetabolic and inflammatory reactions after burns.…”