White matter damage after traumatic brain injury: A role for damage associated molecular patterns

Molly Braun, Kumar Vaibhav, Nancy M. Saad, Sumbul Fatima, John R. Vender, Babak Baban, Md Nasrul Hoda, Krishnan M. Dhandapani

Research output: Contribution to journalReview article

15 Citations (Scopus)

Abstract

Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.

Original languageEnglish (US)
Pages (from-to)2614-2626
Number of pages13
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1863
Issue number10
DOIs
StatePublished - Oct 2017

Fingerprint

Wounds and Injuries
HMGB1 Protein
Pattern Recognition Receptors
Purinergic Receptors
S100 Proteins
Traumatic Brain Injury
White Matter
Toll-Like Receptors
Adaptive Immunity
Hyaluronic Acid
Adenosine Triphosphate
Macrophages
Morbidity
Mortality
Therapeutics
Neuroprotection

Keywords

  • HMGB1
  • Leukocyte
  • Lymphocyte
  • Macrophage
  • Microglia
  • Oligodendrocyte
  • S100
  • T-cell
  • Toll like receptor
  • White matter injury

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

Cite this

White matter damage after traumatic brain injury : A role for damage associated molecular patterns. / Braun, Molly; Vaibhav, Kumar; Saad, Nancy M.; Fatima, Sumbul; Vender, John R.; Baban, Babak; Hoda, Md Nasrul; Dhandapani, Krishnan M.

In: Biochimica et Biophysica Acta - Molecular Basis of Disease, Vol. 1863, No. 10, 10.2017, p. 2614-2626.

Research output: Contribution to journalReview article

@article{7e31e0e4e58249438d97c049a2de117e,
title = "White matter damage after traumatic brain injury: A role for damage associated molecular patterns",
abstract = "Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.",
keywords = "HMGB1, Leukocyte, Lymphocyte, Macrophage, Microglia, Oligodendrocyte, S100, T-cell, Toll like receptor, White matter injury",
author = "Molly Braun and Kumar Vaibhav and Saad, {Nancy M.} and Sumbul Fatima and Vender, {John R.} and Babak Baban and Hoda, {Md Nasrul} and Dhandapani, {Krishnan M.}",
year = "2017",
month = "10",
doi = "10.1016/j.bbadis.2017.05.020",
language = "English (US)",
volume = "1863",
pages = "2614--2626",
journal = "Biochimica et Biophysica Acta - Molecular Basis of Disease",
issn = "0925-4439",
publisher = "Elsevier",
number = "10",

}

TY - JOUR

T1 - White matter damage after traumatic brain injury

T2 - A role for damage associated molecular patterns

AU - Braun, Molly

AU - Vaibhav, Kumar

AU - Saad, Nancy M.

AU - Fatima, Sumbul

AU - Vender, John R.

AU - Baban, Babak

AU - Hoda, Md Nasrul

AU - Dhandapani, Krishnan M.

PY - 2017/10

Y1 - 2017/10

N2 - Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.

AB - Traumatic brain injury (TBI) is a leading cause of mortality and long-term morbidity worldwide. Despite decades of pre-clinical investigation, therapeutic strategies focused on acute neuroprotection failed to improve TBI outcomes. This lack of translational success has necessitated a reassessment of the optimal targets for intervention, including a heightened focus on secondary injury mechanisms. Chronic immune activation correlates with progressive neurodegeneration for decades after TBI; however, significant challenges remain in functionally and mechanistically defining immune activation after TBI. In this review, we explore the burgeoning evidence implicating the acute release of damage associated molecular patterns (DAMPs), such as adenosine 5′-triphosphate (ATP), high mobility group box protein 1 (HMGB1), S100 proteins, and hyaluronic acid in the initiation of progressive neurological injury, including white matter loss after TBI. The role that pattern recognition receptors, including toll-like receptor and purinergic receptors, play in progressive neurological injury after TBI is detailed. Finally, we provide support for the notion that resident and infiltrating macrophages are critical cellular targets linking acute DAMP release with adaptive immune responses and chronic injury after TBI. The therapeutic potential of targeting DAMPs and barriers to clinical translational, in the context of TBI patient management, are discussed.

KW - HMGB1

KW - Leukocyte

KW - Lymphocyte

KW - Macrophage

KW - Microglia

KW - Oligodendrocyte

KW - S100

KW - T-cell

KW - Toll like receptor

KW - White matter injury

UR - http://www.scopus.com/inward/record.url?scp=85020928520&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85020928520&partnerID=8YFLogxK

U2 - 10.1016/j.bbadis.2017.05.020

DO - 10.1016/j.bbadis.2017.05.020

M3 - Review article

C2 - 28533056

AN - SCOPUS:85020928520

VL - 1863

SP - 2614

EP - 2626

JO - Biochimica et Biophysica Acta - Molecular Basis of Disease

JF - Biochimica et Biophysica Acta - Molecular Basis of Disease

SN - 0925-4439

IS - 10

ER -