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. 2020 Jun 1;9(6):1667.
doi: 10.3390/jcm9061667.

Severe Traumatic Brain Injury (TBI) Modulates the Kinetic Profile of the Inflammatory Response of Markers for Neuronal Damage

Cora Rebecca Schindler  1 , Thomas Lustenberger  1 , Mathias Woschek  1 , Philipp Störmann  1 , Dirk Henrich  1 , Peter Radermacher  2 , Ingo Marzi  1
Affiliations

Severe Traumatic Brain Injury (TBI) Modulates the Kinetic Profile of the Inflammatory Response of Markers for Neuronal Damage

Cora Rebecca Schindler et al. J Clin Med. .

Abstract

The inflammatory response plays an important role in the pathophysiology of multiple injuries. This study examines the effects of severe trauma and inflammatory response on markers of neuronal damage. A retrospective analysis of prospectively collected data in 445 trauma patients (Injury Severity Score (ISS) ≥ 16) is provided. Levels of neuronal biomarkers (calcium-binding Protein B (S100b), Enolase2 (NSE), glial fibrillary acidic protein (GFAP)) and Interleukins (IL-6, IL-10) in severely injured patients (with polytrauma (PT)) without traumatic brain injury (TBI) or with severe TBI (PT+TBI) and patients with isolated TBI (isTBI) were measured upon arrival until day 5. S100b, NSE, GFAP levels showed a time-dependent decrease in all cohorts. Their expression was higher after multiple injuries (p = 0.038) comparing isTBI. Positive correlation of marker level after concomitant TBI and isTBI (p = 0.001) was noted, while marker expression after PT appears to be independent. Highest levels of IL-6 and -10 were associated to PT und lowest to isTBI (p < 0.001). In all groups pro-inflammatory response (IL-6/-10 ratio) peaked on day 2 and at a lower level on day 4. Severe TBI modulates kinetic profile of inflammatory response by reducing interleukin expression following trauma. Potential markers for neuronal damage have a limited diagnostic value after severe trauma because undifferentiated increase.

Keywords: GFAP; IL-10; IL-6; NSE; S100b; biomarker; multiple trauma; posttraumatic inflammation; risk prediction; traumatic brain injury (TBI).

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Conflict of interest statement

C. R. Schindler, T. Lustenberger, M. Woschek, P. Störmann, D. Henrich, P. Radermacher, I. Marzi declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Neuronal serum marker levels (mean ± Standard Deviation) over the time course from admission to Emergency Department (ED) through to hospital day 5 stratified by injury pattern. * p < 0.05, ** p < 0.01, *** p < 0.001. (a) Neuron-specific enolase 2 (NSE) (b); glial fibrillary acidic protein (GFAP); (c) calcium-binding Protein B (S100b).
Figure 2
Figure 2
Inflammatory serum marker levels (mean ± Standard Deviation) over the time course from emergency department (ED) admission through to hospital day 5 stratified by injury pattern. * p < 0.05, ** p < 0.01, *** p < 0.001. (a) Interleukin (IL)-6 (b); Interleukin (IL)-10.
Figure 3
Figure 3
Pro-inflammatory response (Interleukin (IL)-6/Interleukin (IL)-10 ratio, grey-hatched) and neuronal marker expression (Neuron-specific enolase 2 (NSE), glial fibrillary acidic protein (GFAP), calcium-binding Protein B (S100b)) after (a) polytrauma (PT); (b) polytrauma + traumatic brain injury (TBI); (c) isolated TBI (isTBI). ED = Admission to Emergency Department.
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