The diagnostic and prognostic value of systems biology research in major traumatic and thermal injury: a review

Abstract

As secondary complications remain a significant cause of morbidity and mortality amongst hospitalised trauma patients, the need to develop novel approaches by which to identify patients at risk of adverse outcome is becoming increasingly important. Centred on the idea that patients who experience “poor” outcome post trauma elicit a response to injury that is distinct from those who experience “good” outcome, tailored therapeutics is an emerging concept aimed at improving current treatment regimens by promoting patient-specific therapies. Making use of recent advancements in the fields of genomics, proteomics and metabolomics, numerous groups have undertaken a systems-based approach to analysing the acute immune and inflammatory response to major traumatic and thermal injury in an attempt to uncover a single or combination of biomarkers that can identify patients at risk of adverse outcome. Early results are encouraging, with all three approaches capable of discriminating patients with “good” outcome from those who develop nosocomial infections, sepsis and multiple organ failure, with differences apparent in blood samples acquired as early as 2 h post injury. In particular, genomic data is proving to be highly informative, identifying patients at risk of “poor” outcome with a higher degree of sensitivity and specificity than statistical models built upon data obtained from existing anatomical and physiological scoring systems. Here, focussing predominantly upon human-based research, we provide an overview of the findings of studies that have investigated the immune and inflammatory response to major traumatic and thermal injury at the genomic, protein and metabolite level, and consider both the diagnostic and prognostic potential of these approaches.

Fractional laser exposure induces neutrophil infiltration (N1 phenotype) into the tumor and stimulates systemic anti-tumor immune response

“…In our study, aFP induced a Treg level decrease. We hypothesize the following meachanism: (1) necrotic and apoptotic tumor cell caused by thermal injury of aFP lead to tumor reduction and release of damage-associated molecular patterns (DAMPs) [ 47 ]. DAMPs recruits neutrophils into the tumor [ 48 ] and lead the recruited neutrophil to shift to N1 phenotype [ 23 ].…”

Astragaloside-IV Alleviates Heat-Induced Inflammation by Inhibiting Endoplasmic Reticulum Stress and Autophagy

“…Furthermore, there should be more signaling pathway in crosstalk between ER stress, autophagy, and inflammatory reactions after heat exposure which we should focus in the furture. And the immune system was reported to be closely related with the inflammation and involved in the anti-inflammatory effect of AS-IV [36], which was needed the further research in the future.…”

Prehospital immune responses and development of multiple organ dysfunction syndrome following traumatic injury: A prospective cohort study

“…Two opposing clinical syndromes characterise the immune and inflammatory response to traumatic injury: systemic inflammatory response syndrome (SIRS), characterised by elevated levels of circulating proinflammatory cytokines and immune cell activation, and compensatory anti-inflammatory response syndrome (CARS), characterised by raised anti-inflammatory cytokines and immuneparesis [2]. The immune response that develops during the SIRS and CARS responses is complex and involves the innate and adaptive arms of the immune system, with significant alterations apparent in the composition, phenotype, and/or function of the circulating immune cell pools.…”