Monitoring the neuroinflammatory response following acute brain injury

Eric Peter Thelin, Tamara Tajsic, Frederick Adam Zeiler, David K Menon, Peter J.A. Hutchinson, Keri L.H. Carpenter, Maria Cristina Morganti-Kossmann, Adel Helmy

Research output: Contribution to journalReview ArticleResearchpeer-review

Abstract

Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are major contributors to morbidity and mortality. Following the initial insult, patients may deteriorate due to secondary brain damage. The underlying molecular and cellular cascades incorporate components of the innate immune system. There are different approaches to assess and monitor cerebral inflammation in the neuro intensive care unit. The aim of this narrative review is to describe techniques to monitor inflammatory activity in patients with TBI and SAH in the acute setting. The analysis of pro- and anti-inflammatory cytokines in compartments of the central nervous system (CNS), including the cerebrospinal fluid and the extracellular fluid, represent the most common approaches to monitor surrogate markers of cerebral inflammatory activity. Each of these compartments has a distinct biology that reflects local processes and the cross-talk between systemic and CNS inflammation. Cytokines have been correlated to outcomes as well as ongoing, secondary injury progression. Alongside the dynamic, focal assay of humoral mediators, imaging, through positron emission tomography, can provide a global in vivo measurement of inflammatory cell activity, which reveals long-lasting processes following the initial injury. Compared to the innate immune system activated acutely after brain injury, the adaptive immune system is likely to play a greater role in the chronic phase as evidenced by T-cell-mediated autoreactivity toward brain-specific proteins. The most difficult aspect of assessing neuroinflammation is to determine whether the processes monitored are harmful or beneficial to the brain as accumulating data indicate a dual role for these inflammatory cascades following injury. In summary, the inflammatory component of the complex injury cascade following brain injury may be monitored using different modalities. Using a multimodal monitoring approach can potentially aid in the development of therapeutics targeting different aspects of the inflammatory cascade and improve the outcome following TBI and SAH.

Original languageEnglish
Article number351
Pages (from-to)1-14
Number of pages14
JournalFrontiers in Neurology
Volume8
Issue numberJUL
DOIs
Publication statusPublished - 20 Jul 2017

Keywords

  • Multimodal monitoring
  • Neuroinflammation
  • Secondary brain injury
  • Subarachnoid hemorrhage
  • Traumatic brain injury

Cite this

Thelin, E. P., Tajsic, T., Zeiler, F. A., Menon, D. K., Hutchinson, P. J. A., Carpenter, K. L. H., ... Helmy, A. (2017). Monitoring the neuroinflammatory response following acute brain injury. Frontiers in Neurology, 8(JUL), 1-14. [351]. https://doi.org/10.3389/fneur.2017.00351
Thelin, Eric Peter ; Tajsic, Tamara ; Zeiler, Frederick Adam ; Menon, David K ; Hutchinson, Peter J.A. ; Carpenter, Keri L.H. ; Morganti-Kossmann, Maria Cristina ; Helmy, Adel. / Monitoring the neuroinflammatory response following acute brain injury. In: Frontiers in Neurology. 2017 ; Vol. 8, No. JUL. pp. 1-14.
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Thelin, EP, Tajsic, T, Zeiler, FA, Menon, DK, Hutchinson, PJA, Carpenter, KLH, Morganti-Kossmann, MC & Helmy, A 2017, 'Monitoring the neuroinflammatory response following acute brain injury' Frontiers in Neurology, vol. 8, no. JUL, 351, pp. 1-14. https://doi.org/10.3389/fneur.2017.00351

Monitoring the neuroinflammatory response following acute brain injury. / Thelin, Eric Peter; Tajsic, Tamara; Zeiler, Frederick Adam; Menon, David K; Hutchinson, Peter J.A.; Carpenter, Keri L.H.; Morganti-Kossmann, Maria Cristina; Helmy, Adel.

In: Frontiers in Neurology, Vol. 8, No. JUL, 351, 20.07.2017, p. 1-14.

Research output: Contribution to journalReview ArticleResearchpeer-review

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AU - Tajsic, Tamara

AU - Zeiler, Frederick Adam

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AU - Hutchinson, Peter J.A.

AU - Carpenter, Keri L.H.

AU - Morganti-Kossmann, Maria Cristina

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N2 - Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are major contributors to morbidity and mortality. Following the initial insult, patients may deteriorate due to secondary brain damage. The underlying molecular and cellular cascades incorporate components of the innate immune system. There are different approaches to assess and monitor cerebral inflammation in the neuro intensive care unit. The aim of this narrative review is to describe techniques to monitor inflammatory activity in patients with TBI and SAH in the acute setting. The analysis of pro- and anti-inflammatory cytokines in compartments of the central nervous system (CNS), including the cerebrospinal fluid and the extracellular fluid, represent the most common approaches to monitor surrogate markers of cerebral inflammatory activity. Each of these compartments has a distinct biology that reflects local processes and the cross-talk between systemic and CNS inflammation. Cytokines have been correlated to outcomes as well as ongoing, secondary injury progression. Alongside the dynamic, focal assay of humoral mediators, imaging, through positron emission tomography, can provide a global in vivo measurement of inflammatory cell activity, which reveals long-lasting processes following the initial injury. Compared to the innate immune system activated acutely after brain injury, the adaptive immune system is likely to play a greater role in the chronic phase as evidenced by T-cell-mediated autoreactivity toward brain-specific proteins. The most difficult aspect of assessing neuroinflammation is to determine whether the processes monitored are harmful or beneficial to the brain as accumulating data indicate a dual role for these inflammatory cascades following injury. In summary, the inflammatory component of the complex injury cascade following brain injury may be monitored using different modalities. Using a multimodal monitoring approach can potentially aid in the development of therapeutics targeting different aspects of the inflammatory cascade and improve the outcome following TBI and SAH.

AB - Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are major contributors to morbidity and mortality. Following the initial insult, patients may deteriorate due to secondary brain damage. The underlying molecular and cellular cascades incorporate components of the innate immune system. There are different approaches to assess and monitor cerebral inflammation in the neuro intensive care unit. The aim of this narrative review is to describe techniques to monitor inflammatory activity in patients with TBI and SAH in the acute setting. The analysis of pro- and anti-inflammatory cytokines in compartments of the central nervous system (CNS), including the cerebrospinal fluid and the extracellular fluid, represent the most common approaches to monitor surrogate markers of cerebral inflammatory activity. Each of these compartments has a distinct biology that reflects local processes and the cross-talk between systemic and CNS inflammation. Cytokines have been correlated to outcomes as well as ongoing, secondary injury progression. Alongside the dynamic, focal assay of humoral mediators, imaging, through positron emission tomography, can provide a global in vivo measurement of inflammatory cell activity, which reveals long-lasting processes following the initial injury. Compared to the innate immune system activated acutely after brain injury, the adaptive immune system is likely to play a greater role in the chronic phase as evidenced by T-cell-mediated autoreactivity toward brain-specific proteins. The most difficult aspect of assessing neuroinflammation is to determine whether the processes monitored are harmful or beneficial to the brain as accumulating data indicate a dual role for these inflammatory cascades following injury. In summary, the inflammatory component of the complex injury cascade following brain injury may be monitored using different modalities. Using a multimodal monitoring approach can potentially aid in the development of therapeutics targeting different aspects of the inflammatory cascade and improve the outcome following TBI and SAH.

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Thelin EP, Tajsic T, Zeiler FA, Menon DK, Hutchinson PJA, Carpenter KLH et al. Monitoring the neuroinflammatory response following acute brain injury. Frontiers in Neurology. 2017 Jul 20;8(JUL):1-14. 351. https://doi.org/10.3389/fneur.2017.00351