Abstract
Time-dependent changes in blood-based protein biomarkers can help identify the pathological processes in blast-induced traumatic brain injury (bTBI), assess injury severity, and monitor disease progression. We obtained blood from control and injured mice (exposed to a single, low-intensity blast) at 2-h, 1-day, 1–week, and 1-month post-injury. We then determined the serum levels of biomarkers related to metabolism (4-HNE, HIF-1α, ceruloplasmin), vascular function (AQP1, AQP4, VEGF, vWF, Flk-1), inflammation (OPN, CINC1, fibrinogen, MIP-1a, OX-44, p38, MMP-8, MCP-1 CCR5, CRP, galectin-1), cell adhesion and the extracellular matrix (integrin α6, TIMP1, TIMP4, Ncad, connexin-43), and axonal (NF-H, Tau), neuronal (NSE, CK-BB) and glial damage (GFAP, S100β, MBP) at various post-injury time points. Our findings indicate that the exposure to a single, low-intensity blast results in metabolic and vascular changes, altered cell adhesion, and axonal and neuronal injury in the mouse model of bTBI. Interestingly, serum levels of several inflammatory and astroglial markers were either unchanged or elevated only during the acute and subacute phases of injury. Conversely, serum levels of the majority of biomarkers related to metabolic and vascular functions, cell adhesion, as well as neuronal and axonal damage remained elevated at the termination of the experiment (1 month), indicating long-term systemic and cerebral alterations due to blast. Our findings show that the exposure to a single, low-intensity blast induces complex pathological processes with distinct temporal profiles. Hence, monitoring serum biomarker levels at various post-injury time points may provide enhanced diagnostics in blast-related neurological and multi-system deficits.
Highlights
IntroductionThe mild form of traumatic brain injury (mTBI, called concussion) accounts for ~75% of all head injuries among civilians and military personnel [1, 2]
The mild form of traumatic brain injury accounts for ~75% of all head injuries among civilians and military personnel [1, 2]
The neurological deficits that develop after blast exposure(s) are resulted from the brain damage caused via head-blast interaction and from multiple, synergistically acting injury mechanisms
Summary
The mild form of traumatic brain injury (mTBI, called concussion) accounts for ~75% of all head injuries among civilians and military personnel [1, 2]. Temporal changes of bTBI biomarkers blast TBI (bTBI), have been coined to describe the unique clinical entity of blast-induced neurological deficits caused by interwoven mechanisms of systemic, local, and cerebral responses to blast exposure(s) [4, 5]. The neurological deficits that develop after blast exposure(s) are resulted from the brain damage caused via head-blast interaction and from multiple, synergistically acting injury mechanisms. Because of such complexity, the diagnosis of blast-induced neurological consequences, both during the acute and chronic injury phases, is extremely challenging: the manifestations of mbTBI are often masked by symptoms of systemic changes
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