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<p>Traumatic brain injury (TBI) represents a neuropathological entity with multifactorial consequences, encompassing immediate mechanical insult (primary injury) and a complex and temporally dynamic cascade of secondary injury mechanisms. Despite increasing interest in the proteomic and transcriptomic characterization of TBI-related neuroinflammation, systematic investigations integrating peripheral and central compartments in human post-mortem samples are limited. The few available studies often rely on single-modality approaches, limiting their ability to capture the full spectrum of neuroinflammatory signatures. The aim of this study was to clarify whether increased levels of TNF-α and CX3CL1 in biofluids, including serum and cerebrospinal fluid (CSF), are detected in cases of TBI in an autopsy-based population analysis. The equivalent analysis of TNFR1, TNFR2, and CX3CR1 protein expression in the harvested brain tissue through immunohistochemical staining was additionally performed. All 40 cases in the study were split into two groups: those with severe head injuries (<i>n</i> = 20) that were thought to be the cause of death, and control atraumatic instances of sudden death (<i>n</i> = 20) from cardiac causes. About 24&#xa0;h after the lethal incident, bodily fluids, such as serum and CSF, were collected and subjected to ELISA testing. Immunohistochemical staining was also applied to brain tissue collected during additional neuropathological examinations. In the present study, we observed the elevated concentration level of TNF-α and CX3CL1 in CSF, without its clear elevation within serum. In the frontal cortex and hippocampus, homogenized and intensified staining of all receptors across neuronal structures, including somata, axons, and nuclear regions, was observed in the study group. In conclusion, this study presents novel post-mortem data on neuroinflammatory dynamics in a rigorously defined population following lethal TBI, highlighting significant up-regulation of TNF-α and CX3CL1 in CSF, and distinct immunohistochemical remodeling of TNFR1, TNFR2, and CX3CR1 in vulnerable brain regions. The encouraging use of TNF-α, CX3CL1, TNFR1, TNFR2, and CX3CR1 assays offers a potential application for investigation and research regarding TBI diagnosis and pathogenesis.</p>

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Utility of selected neuroinflammatory markers following lethal traumatic brain injury: a combined biofluid and tissue-based assessment of TNF-α, CX3CL1, TNFR1, TNFR2 and CX3CR1 expression

  • 期刊论文

  • 发表日期：

    2026年4月23日

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  • Łukasz A. Poniatowski,
  • Magdalena Kwiatkowska,
  • Agnieszka Siwińska,
  • Albert Acewicz,
  • Mieszko Olczak

摘要

Traumatic brain injury (TBI) represents a neuropathological entity with multifactorial consequences, encompassing immediate mechanical insult (primary injury) and a complex and temporally dynamic cascade of secondary injury mechanisms. Despite increasing interest in the proteomic and transcriptomic characterization of TBI-related neuroinflammation, systematic investigations integrating peripheral and central compartments in human post-mortem samples are limited. The few available studies often rely on single-modality approaches, limiting their ability to capture the full spectrum of neuroinflammatory signatures. The aim of this study was to clarify whether increased levels of TNF-α and CX3CL1 in biofluids, including serum and cerebrospinal fluid (CSF), are detected in cases of TBI in an autopsy-based population analysis. The equivalent analysis of TNFR1, TNFR2, and CX3CR1 protein expression in the harvested brain tissue through immunohistochemical staining was additionally performed. All 40 cases in the study were split into two groups: those with severe head injuries (n = 20) that were thought to be the cause of death, and control atraumatic instances of sudden death (n = 20) from cardiac causes. About 24 h after the lethal incident, bodily fluids, such as serum and CSF, were collected and subjected to ELISA testing. Immunohistochemical staining was also applied to brain tissue collected during additional neuropathological examinations. In the present study, we observed the elevated concentration level of TNF-α and CX3CL1 in CSF, without its clear elevation within serum. In the frontal cortex and hippocampus, homogenized and intensified staining of all receptors across neuronal structures, including somata, axons, and nuclear regions, was observed in the study group. In conclusion, this study presents novel post-mortem data on neuroinflammatory dynamics in a rigorously defined population following lethal TBI, highlighting significant up-regulation of TNF-α and CX3CL1 in CSF, and distinct immunohistochemical remodeling of TNFR1, TNFR2, and CX3CR1 in vulnerable brain regions. The encouraging use of TNF-α, CX3CL1, TNFR1, TNFR2, and CX3CR1 assays offers a potential application for investigation and research regarding TBI diagnosis and pathogenesis.