Traumatic brain injury and neuroinflammation: Review of the main biomarkers

Abstract

Traumatic brain injury is one of the main causes of both acute and long-term morbidity that concern that affects individuals in all demographics. The processes that occur during traumatic brain injury and neuroinflammation cannot be fully explained in most clinical and preclinical researches. Neuroinflammation is a very complex interaction between the cells of the innate and adaptive immune systems. The development of reactions of the innate immune system occurs under the influence of various signals that are released from damaged cells and tissues. This leads to the activation of neutrophils, microglia and astrocytes, the release of complement, as well as the release of histamine by mast cells. Subsequently, activation of an adaptive immune response leads to the development of later effects of neuroinflammation. The topic of biomarkers in traumatic brain injury is extensive and rapidly developing. We presented an overview of the most common and well-studied biomarkers in the literature regarding head injury in humans and their role in predicting the outcome in traumatic brain injury. Among the presented biomarkers, the most specific for traumatic brain injury are interleukins-6, -8, -10 and matrix metalloproteinases. We can use interleukin-6 to predict the outcome and risk of complications of traumatic brain injury. The concentration of interleukin-8 shows the relationship of the biomarker with mortality. We can use interleukin-10 to confirm the results of computed tomography in traumatic brain injury. Matrix metalloproteinases present the degree of violation of the blood-brain barrier and brain dysfunction. Other indicators need a more complete study to clarify their role in this pathology. Of course, for a more reliable conclusion about the patient's condition, it is preferable to use the data of several biomarkers at the same time. © 2012 Scientific Centre for Family Health and Human Reproduction Problems. All Rights Reserved.