Cited by 278Traumatic Brain Injury and Neurovascular DisturbancesTraumatic Brain Injury ResearchNeuroinflammation and Neurodegeneration Mechanisms

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In Situ Detection of Inflammatory Mediators in Post Mortem Human Brain Tissue after Traumatic Injury

Frugier, Tony, Morganti-Kossmann, Maria Cristina, O'Reilly, David, McLean, Catriona A.·2010·Journal of Neurotrauma

DOI 10.1089/neu.2009.1120

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Abstract

Little is known about the molecular events following severe traumatic brain injury (TBI) in humans and to date there are no efficient therapies for the treatment of patients. In this study, the first of its kind in human tissue, a total of 21 post mortem trauma brain samples were analyzed. The inflammatory response within the brain tissue was explored by measuring the expression of various inflammatory cytokines at the mRNA and protein levels. These mediators were interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and granulocyte-macrophage colony-stimulating factor (GM-CSF). This study shows for the first time in human brain tissue that 1) pro-inflammatory mediator protein levels are significantly increased in situ following acute brain injury while anti-inflammatory cytokines protein levels remain unchanged; 2) the cerebral inflammatory response begins within minutes of acute TBI, much earlier than previously thought; 3) IL-6, IL-8, TNF-alpha, and IL-1beta mRNA levels are significantly increased following injury; 4) the rise in cytokine protein level coincides with increased levels of their mRNAs suggesting that traumatic injury elicits an immediate cerebral inflammatory response. Altogether these data confirm and extend previous observations on the release of cytokines in the cerebrospinal fluid of severe TBI patients. Finally, this study highlights the need to characterize the cell source of cytokines and elucidate their mode of action.

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Taylor, D. D., & Gerçel-Taylor, Ç. (2014) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2013.0503 · Cited by 85
“Investigators have shown the presence of TNF-a protein and mRNA at the sites of traumatic lesions within minutes and the TNF-a concentrations peak in the cerebrospinal fluid (CSF) within 24 h [21,22].”
Background
Texture analysis of MR images of patients with Mild Traumatic Brain Injury
Holli, K. K., Harrison, L., Dastidar, P., Wäljas, M., Liimatainen, S., Luukkaala, T. H., Öhman, J. E., Soimakallio, S., & Eskola, H. J. (2010) · BMC Medical Imaging · doi:10.1186/1471-2342-10-8 · Cited by 81
Considerations for Experimental Animal Models of Concussion, Traumatic Brain Injury, and Chronic Traumatic Encephalopathy—These Matters Matter
Wojnarowicz, M. W., Fisher, A. M., Minaeva, O. V., & Goldstein, L. E. (2017) · Frontiers in Neurology · doi:10.3389/fneur.2017.00240 · Cited by 85
Traumatic brain injury triggers APP and Tau cleavage by delta-secretase, mediating Alzheimer’s disease pathology
Wu, Z., Wang, Z.-H., Liu, X., Zhang, Z., Gu, X., Yu, S. P., Keene, C. D., Cheng, L., & Ye, K. (2019) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2019.101730 · Cited by 81
Diffuse Brain Injury Induces Acute Post-Traumatic Sleep
Rowe, R. K., Striz, M., Bachstetter, A., Eldik, L. V. V., Donohue, K., O'Hara, B., & Lifshitz, J. (2014) · PLoS ONE · doi:10.1371/journal.pone.0082507 · Cited by 84
“Following brain injury there is an up-regulation of proinflammatory cytokines [30] that include IL-1b [12,18].”
Depression following a traumatic brain injury: uncovering cytokine dysregulation as a pathogenic mechanism
Bachstetter, A. D., Bodnar, C., & Morganti, J. M. (2018) · Neural Regeneration Research · doi:10.4103/1673-5374.238604 · Cited by 85
“…al., 2007; Chiaretti et al., 2008; Helmy et al., 2011; Mellergard et al., 2011; Roberts et al., 2013; Nwachuku et al., 2016), while not in others (Frugier et al., 2010; Aisiku et al., 2016; Kumar et al., 2016) The increases in cytokine levels occurring acutely after injury, as measured in the…”
A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis
Jackson, T. C., & Kochanek, P. M. (2019) · Therapeutic Hypothermia and Temperature Management · doi:10.1089/ther.2019.0001 · Cited by 77
“Liberation of intracellular DNA and debris from dying cells into the extracellular space, and release of additional damage-associated molecular patterns (DAMPs), triggers an immediate (within minutes/h) proinflammatory cytokine response in the brain (e.g., increased TNF, IFNc, and IL-6) (Frugier et al., 2010; Ansari,…”
Background
Neutrophil-to-Lymphocyte Ratio and Traumatic Brain Injury: A Review Study
Sabouri, E., Majdi, A., Jangjui, P., Aghsan, S. R., & Alavi, S. A. N. (2020) · World Neurosurgery · doi:10.1016/j.wneu.2020.04.185 · Cited by 77
Neuroinflammation in HIV-associated depression: evidence and future perspectives
Rakshasa-Loots, A. M., Whalley, H. C., Vera, J. H., & Cox, S. R. (2022) · Molecular Psychiatry · doi:10.1038/s41380-022-01619-2 · Cited by 77
“However, brain biopsies are highly invasive and generally cannot be justified in research studies, whereas histopathological analyses in humans are limited by availability of post-mortem brain tissue samples [27, 28].”
Astrocyte Hypertrophy Contributes to Aberrant Neurogenesis after Traumatic Brain Injury
Robinson, C., Apgar, C. J., & Shapiro, L. A. (2016) · Neural Plasticity · doi:10.1155/2016/1347987 · Cited by 72
Melatonin as a Potential Regulator of Oxidative Stress, and Neuroinflammation: Mechanisms and Implications for the Management of Brain Injury-Induced Neurodegeneration
Ikram, M. A., Park, H. Y., Ali, T., & Kim, M. O. (2021) · Journal of Inflammation Research · doi:10.2147/jir.s334423 · Cited by 70
“Traumatic Brain Injury and Neuroinflammation Within 24 hours of TBI, the permeability of the blood-brain barrier (BBB) increases the infiltration of circulating monocytes, neutrophils, and lymphocytes into the brain parenchyma,(34) which activates the complement system and release inflammatory cytokines such as tissue…”
Background
Photobiomodulation for the treatment of neuroinflammation: A systematic review of controlled laboratory animal studies
Cardoso, F. D. S., Salehpour, F., Coimbra, N. C., Gonzalez-Lima, F., & da Silva, S. G. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.1006031 · Cited by 73
“In addition, the release of these cytokines was correlated with microglial activation and axonal dysfunction, suggesting an association between the activated immune response and brain injury (Frugier et al., 2010).”
Background
A blood-based biomarker panel to risk-stratify mild traumatic brain injury
Sharma, R., Rosenberg, A., Bennett, E. R., Laskowitz, D. T., & Acheson, S. K. (2017) · PLoS ONE · doi:10.1371/journal.pone.0173798 · Cited by 66
Granulocyte-Macrophage Colony-Stimulating Factor Is Neuroprotective in Experimental Traumatic Brain Injury
Shultz, S. R., Tan, X. L., Wright, D. K., Liu, S. J., Semple, B. D., Johnston, L. A., Jones, N. C., Cook, A. D., Hamilton, J. A., & O'Brien, T. J. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3106 · Cited by 66
Metabolomics and Biomarker Discovery in Traumatic Brain Injury
Banoei, M. M., Casault, C. A., Metwaly, S., & Winston, B. W. (2018) · Journal of Neurotrauma · doi:10.1089/neu.2017.5326 · Cited by 68
Cytokine Gene Polymorphisms and Outcome after Traumatic Brain Injury
Waters, R. J., Murray, G. D., Teasdale, G. M., Stewart, J., Day, I. N. M., Lee, R. J., & Nicoll, J. A. R. (2013) · Journal of Neurotrauma · doi:10.1089/neu.2012.2792 · Cited by 65
Neurotrauma: The Crosstalk between Neurotrophins and Inflammation in the Acutely Injured Brain
Meirelles, L. D. S., Simon, D., & Regner, A. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18051082 · Cited by 68
The closed-head impact model of engineered rotational acceleration (CHIMERA) as an application for traumatic brain injury pre-clinical research: A status report.
McNamara, E. H., Grillakis, A., Tucker, L. B., & McCabe, J. (2020) · Experimental Neurology · doi:10.1016/j.expneurol.2020.113409 · Cited by 61
“Inflammation Inflammation after traumatic brain injury has been characterized in animal models as well as in clinical populations (Corps et al., 2015; Frugier et al., 2010).”
The Bidirectional Relationship Between Sleep and Inflammation Links Traumatic Brain Injury and Alzheimer’s Disease
Green, T. R. F., Ortiz, J. B., Wonnacott, S., Williams, R. J., & Rowe, R. K. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.00894 · Cited by 68
“Using these techniques, waves of CSF flow were observed during slow wave sleep, which appeared to be coupled with the hemodynamic rhythm during sleep (Fultz et al., 2019).”
Method
Allyl isothiocyanate attenuates oxidative stress and inflammation by modulating Nrf2/HO-1 and NF-κB pathways in traumatic brain injury in mice
Çağlayan, B., Kılıç, E., Dalay, A., Altunay, S., Tuzcu, M., Erten, F., Orhan, C., Günal, M. Y., Yuluğ, B., Juturu, V., et al. (2018) · Molecular Biology Reports · doi:10.1007/s11033-018-4465-4 · Cited by 64
Mild Chronic Traumatic Encephalopathy Neuropathology in People With No Known Participation in Contact Sports or History of Repetitive Neurotrauma
Iverson, G. L., Luoto, T. M., Karhunen, P. J., & Castellani, R. J. (2019) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlz045 · Cited by 63
“There are other studies, however, indicating that different types of neuropathology, such as neuroinflammation (36), b-amyloid deposition (37), and accumulation of TDP-43 (38) and p-tau (37, 39, 40) can and do arise following a single moderate-severe TBI (41–43), and there is emerging evidence that multiple types of n…”
Background
Roles of fatty acid ethanolamides (FAE) in traumatic and ischemic brain injury
Esposito, E., Cordaro, M., & Cuzzocrea, S. (2014) · Pharmacological Research · doi:10.1016/j.phrs.2014.05.009 · Cited by 61
Ablation of Type-1 IFN Signaling in Hematopoietic Cells Confers Protection Following Traumatic Brain Injury
Karve, I. P., Zhang, M., Habgood, M. D., Frugier, T., Brody, K. M., Sashindranath, M., Ek, C. J., Chappaz, S., Kile, B. T., Wright, D. K., et al. (2016) · eNeuro · doi:10.1523/eneuro.0128-15.2016 · Cited by 64
“Trauma brain samples from individuals who had died following closed head injury and non-head trauma controls were obtained from the Victorian Brain Bank Network (Frugier et al., 2010, 2011,2012).”
Method
IL6 deficiency affects function after traumatic brain injury.
Ley, E. J., Clond, M. A., Singer, M., Shouhed, D., & Salim, A. (2011) · Journal of Surgical Research · doi:10.1016/j.jss.2011.03.006 · Cited by 57
“After TBI, IL6 is elevated in brain tissue [4], cerebrospinal fluid, and serum [5], and is thus recognized as a highly specific biomarker of injury severity and long-term outcome [6].”
Background
Interferons in Traumatic Brain and Spinal Cord Injury: Current Evidence for Translational Application
Roselli, F., Chandrasekar, A., & Morganti-Kossmann, M. C. (2018) · Frontiers in Neurology · doi:10.3389/fneur.2018.00458 · Cited by 60
“Interestingly, the area of the cortex used for cytokine analysis also presented astrogliosis and macrophage activation located in proximity to axonal pathology, implying a direct link between cellular and humoral inflammation (40).”
Recovery of neurological function despite immediate sleep disruption following diffuse brain injury in the mouse: clinical relevance to medically untreated concussion.
Rowe, R. K., Harrison, J., O'Hara, B., & Lifshitz, J. (2014) · Sleep · doi:10.5665/sleep.3582 · Cited by 62
Neuroprotective Effect of Oridonin on Traumatic Brain Injury via Inhibiting NLRP3 Inflammasome in Experimental Mice
Yan, C., Yan, H., Mao, J., Liu, Y., Li, X., Zhao, H., Shen, J., Cao, Y. W., Gao, Y., Li, K., et al. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.557170 · Cited by 58
Biomarkers in Traumatic Brain Injury
Sharma, R., & Laskowitz, D. (2012) · Current Neurology and Neuroscience Reports · doi:10.1007/s11910-012-0301-8 · Cited by 36
“It is possible that these cytokines are being secreted by a CNS source, since TNF-α, IL-6, IL-8, IL-10, and TGF-β detected in CSF are significantly higher than levels seen in serum [20].”
BackgroundInfluential
Aged rats have an altered immune response and worse outcomes after traumatic brain injury
Sun, M., Brady, R. D., Casillas-Espinosa, P. M., Wright, D. K., Semple, B. D., Kim, H. A., Mychasiuk, R., Sobey, C. G., O'Brien, T. J., Vinh, A., et al. (2019) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2019.04.038 · Cited by 59
Ceruloplasmin and β-amyloid precursor protein confer neuroprotection in traumatic brain injury and lower neuronal iron
Ayton, S., Zhang, M., Roberts, B. R., Lam, L. Q., Lind, M., McLean, C., Bush, A. I., Frugier, T., Crack, P. J., & Duce, J. A. (2014) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2014.01.041 · Cited by 56
“previously reported[25-27], the human cortical brain region analysed was located within 1 cm of the injured tissue and was identified macroscopically by a neuropathologist (Prof.”
Background
Evaluation of M2-like macrophage enrichment after diffuse traumatic brain injury through transient interleukin-4 expression from engineered mesenchymal stromal cells
Enam, S. F., Kader, S. R., Bodkin, N., Lyon, J. G., Calhoun, M. A., Azrak, C., Tiwari, P. M., Vanover, D. A., Wang, H., Santangelo, P. J., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01860-y · Cited by 55
“Unfortunately, IL-4 levels do not increase in humans or mice after TBI [62, 63].”
Background
Hemorrhagic Shock Shifts the Serum Cytokine Profile from Pro- to Anti-Inflammatory after Experimental Traumatic Brain Injury in Mice
Shein, S. L., Shellington, D. K., Exo, J. L., Jackson, T. C., Wisniewski, S. R., Jackson, E. K., Vagni, V., Bayır, H., Clark, R. S. B., Dixon, C. E., et al. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.2985 · Cited by 56
Bifunctional role of pro-inflammatory cytokines after traumatic brain injury
Sordillo, P. P., Sordillo, L. A., & Helson, L. (2016) · Brain Injury · doi:10.3109/02699052.2016.1163618 · Cited by 55
“IL-2 Pro-inflammatory cytokine, T-cell lymphocyte differentiation [63,86,192,193] IL-4 Anti-inflammatory cytokine, also stimulates B-cell proliferation [38,63,86,122,191,192] IL-6 Major pro-inflammatory cytokine, B-cell differentiation, neurogenesis, myokine, also has anti-inflammatory functions (suppression of IL-1 a…”
Background
Exercise attenuates neurological deficits by stimulating a critical HSP70/NF-κB/IL-6/synapsin I axis in traumatic brain injury rats
Chio, C., Lin, H., Tian, Y.-F., Chen, Y., Lin, M., Lin, C., Chang, C., & Hsu, C. (2017) · Journal of Neuroinflammation · doi:10.1186/s12974-017-0867-9 · Cited by 58
“After a TBI, interleukin-6 (IL-6) is also elevated in serum [10], cerebrospinal fluid [11], and brain tissue [12] and is considered a biomarker of TBI outcome [13–15].”
Background
A Rehabilomics focused perspective on molecular mechanisms underlying neurological injury, complications, and recovery after severe TBI
Wagner, A. K., & Zitelli, K. T. (2012) · Pathophysiology · doi:10.1016/j.pathophys.2012.02.007 · Cited by 54
Microglial cell‐derived interleukin‐6 influences behavior and inflammatory response in the brain following traumatic brain injury
Sanchís, P., Fernández‐Gayol, O., Vizueta, J., Comes, G., Canal, C., Escrig, A., Molinero, A., Giralt, M., & Hidalgo, J. (2019) · Glia · doi:10.1002/glia.23758 · Cited by 54
“…phagocytic cells and microglia, and different cytokines, with IL-6 being an important mediator of the inflammatory cascade (Chhor et al., 2017; Frugier et al., 2010; Graber, Costine, & Hickey, 2015; A. Kumar, Alvarez-Croda, Stoica, Faden, & Loane, 2015; Lenzlinger, Morganti-Kossmann, Laurer,…”
Type I Interferon Response Is Mediated by NLRX1-cGAS-STING Signaling in Brain Injury
Fritsch, L. E., Ju, J., Basso, E. K. G., Soliman, E., Paul, S., Chen, J., Kaloss, A. M., Kowalski, E., Tuhy, T. C., Somaiya, R. D., et al. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.852243 · Cited by 54
Chloroquine exerts neuroprotection following traumatic brain injury via suppression of inflammation and neuronal autophagic death
Cui, C., Gao, J., Cui, Y., Sun, L., WANG, Y.-C., Wang, K., Li, R., Tian, Y., & CUI, J.-Z. (2015) · Molecular Medicine Reports · doi:10.3892/mmr.2015.3611 · Cited by 53
“This delayed pathophysiological cascade is now believed to result from a combination of factors, including increases in neurotransmitter release (23), free radical over-production (24), exacerbated inflammatory response (25) and subsequent neuronal cell death via apoptosis and autophagy (8,26).”
Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis
Ziaka, M., & Exadaktylos, A. K. (2024) · Critical Care · doi:10.1186/s13054-024-04855-w · Cited by 54
Hydrogen-rich water attenuates brain damage and inflammation after traumatic brain injury in rats
Tian, R., Hou, Z., Hao, S., Wu, W., Mao, X., Tao, X., Lu, T., & Liu, B. (2016) · Brain Research · doi:10.1016/j.brainres.2016.01.029 · Cited by 52
Expression and Activation of EphA4 in the Human Brain After Traumatic Injury
Frugier, T., Conquest, A., McLean, C., Currie, P. D., Moses, D., & Goldshmit, Y. (2012) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e3182496149 · Cited by 52
“We used samples from the same cohort of patients in 2 previous studies (18, 19).”
BackgroundMethodInfluential
Traumatic Injury Leads to Inflammation and Altered Tryptophan Metabolism in the Juvenile Rabbit Brain
Zhang, Z., Rasmussen, L., Saraswati, M., Koehler, R., Robertson, C., & Kannan, S. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2017.5450 · Cited by 49
How to Translate Time: The Temporal Aspects of Rodent and Human Pathobiological Processes in Traumatic Brain Injury
Agoston, D. V., Vink, R., Helmy, A. E., Risling, M., Nelson, D., & Prins, M. L. (2019) · Journal of Neurotrauma · doi:10.1089/neu.2018.6261 · Cited by 52
“crosis factor (TNF), are significantly increased in the human brain within 24 h after TBI.(50) Subsequent to this early period, once patients are admitted to specialist neurointensive care, invasive”
Background
Sigma-1 Receptor Modulates Neuroinflammation After Traumatic Brain Injury
Dong, H. F., Ma, Y., Ren, Z., Xu, B., Zhang, Y., Chen, J., & Yang, B. (2015) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-015-0244-0 · Cited by 52
Systemic inflammation alters the neuroinflammatory response: a prospective clinical trial in traumatic brain injury
Lassarén, P., Lindblad, C., Frostell, A., Carpenter, K. L. H., Guilfoyle, M. R., Hutchinson, P. J., Helmy, A. E., & Thelin, E. P. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02264-2 · Cited by 53

Authors: Frugier, T., Morganti-Kossmann, M. C., O'Reilly, D., & McLean, C. A.
Affiliations: The Alfred Hospital (AU)
National Trauma Research Institute, The Alfred Hospital and Department of Medicine Monash University, Melbourne, Victoria, Australia.
Corresponding author: Frugier, Tony
ORCID: Frugier, Tony
Morganti-Kossmann, Maria Cristina
McLean, Catriona A.
Venue: Journal of Neurotrauma
Publisher: SAGE Publications
Published: 2010-03
Volume: 27
Issue: 3
Pages: 497-507
ISSN: 0897-7151 (ISSN-L)
1557-9042
DOI: 10.1089/neu.2009.1120
OpenAlex: W2084674974
Cited by: 278
References: 50
Citations by year: 2026: 9 · 2025: 15 · 2024: 21 · 2023: 12 · 2022: 20 · 2021: 23 · 2020: 25 · 2019: 22 · 2018: 16 · 2017: 21 · 2016: 15 · 2015: 15 · 2014: 24 · 2013: 19 · 2012: 14
FWCI: 4.47
Type: journal article
Language: en
Open access: closed
Licence: www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/ (tdm)
Locations: Journal of Neurotrauma (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: traumatic brain injury, neuroinflammation, inflammatory cytokines, postmortem brain, interleukin-6, interleukin-8, TNF-α, IL-1β, cytokine mRNA expression, human brain
MeSH terms: Adolescent, Adult, Aged, Brain, Brain Injuries, Diagnosis, Encephalitis, Female, Humans, Interferon-gamma, Interleukins, Male, Middle Aged, RNA, Messenger, Tumor Necrosis Factor-alpha, Biomarkers, Granulocyte-Macrophage Colony-Stimulating Factor, Cytokines, Inflammation Mediators, Young Adult

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In Situ Detection of Inflammatory Mediators in Post Mortem Human Brain Tissue after Traumatic Injury

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