Neutrophils in traumatic brain injury (TBI): friend or foe?

Liu, Yang‐Wuyue; Li, Song; Dai, Shuang-Shuang

doi:10.1186/s12974-018-1173-x

Cited by 115 publications

(114 citation statements)

References 279 publications

(248 reference statements)

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“…As described previously, circulating NETs activate the coagulation system, increasing viscosity and changing the rheological properties of the blood [72]. Accordingly, changes in CSF hydrodynamics, as a consequence of NET generation in the CSF compartment, may hinder CSF circulation leading to the development of oedema and increased intracranial pressure [73].…”

Section: Cns Infectionsmentioning

confidence: 89%

The Brain Entangled: The Contribution of Neutrophil Extracellular Traps to the Diseases of the Central Nervous System

Manda-Handzlik

Demkow

2019

Cells

107

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Under normal conditions, neutrophils are restricted from trafficking into the brain parenchyma and cerebrospinal fluid by the presence of the brain-blood barrier (BBB). Yet, infiltration of the central nervous system (CNS) by neutrophils is a well-known phenomenon in the course of different pathological conditions, e.g., infection, trauma or neurodegeneration. Different studies have shown that neutrophil products, i.e., free oxygen radicals and proteolytic enzymes, play an important role in the pathogenesis of BBB damage. It was recently observed that accumulating granulocytes may release neutrophil extracellular traps (NETs), which damage the BBB and directly injure surrounding neurons. In this review, we discuss the emerging role of NETs in various pathological conditions affecting the CNS.

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Section: Cns Infectionsmentioning

confidence: 89%

The Brain Entangled: The Contribution of Neutrophil Extracellular Traps to the Diseases of the Central Nervous System

Manda-Handzlik

Demkow

2019

Cells

107

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“…at the lesion area over time, further contributes to BBB damage. Additional cytokine, matrix metallopeptidase (MMP), and reactive oxygen species (ROS) released by activated neutrophils and monocyte/macrophages further disrupt the BBB via down-regulation of tight junction proteins as well as through recruitment of additional inflammatory cells [28,[31][32][33][34]. An overview of the major peripheral immune cell response is depicted in Figure 1.…”

Section: Blood-brain Barrier Compromise and Immune Cell Infiltrationmentioning

confidence: 99%

“…Neutrophils: Neutrophils arrive at the lesion area in the early stages of injurythese cells migrate to the area of injury and infiltrate damaged brain tissue within the first 24 hours postinjury [33]. These cells are recruited by the release of IL-8, a chemoattractant cytokine known to be generated in the early stage of TBI [35].…”

Section: Immune Cell-specific Contribution To Tbimentioning

confidence: 99%

Peripheral Immune Response Following Traumatic Brain Injury

Hazy¹,

Kowalski²,

Groot³

et al. 2021

Advancement and New Understanding in Brain Injury

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Traumatic brain injury (TBI) represents a leading contributor to long-term neurological damage. Though TBI is a leading cause of death and neurological damage worldwide, there exists no therapeutic treatments to alleviate deleterious secondary injury due to neuroinflammation. The continuum of pro-and anti-inflammatory response elicited by TBI is suggested to play a key role in the outcome of TBI; however, the underlying mechanisms remain poorly defined. This chapter explores rodent models of injury used to study the disease pathology of TBI, as well as the major contributions of the peripheral immune response following injury. Further, this chapter discusses the influence of individual immune cell types on neuroinflammation following TBI, focusing on peripheral monocyte/macrophages, their polarization state, and the current literature surrounding their behavior within the TBI milieu. Finally, cell-to-cell contact regulators that effect peripheral-induced neuroinflammation and may serve as novel targets for therapeutics will be highlighted.

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“…As these microglia work to remove the cellular debris at the lesion site, they produce cytokines and chemokines that activate pattern recognition receptors to bind damage‐associated molecular patterns, and attract and polarize peripheral immune cells. The first peripheral immune cells into the damaged tissue are neutrophils followed 24‐48 hours later by monocytes or macrophage, and T cells all of which are releasing cytokines and chemokines. Once the peripheral immune cells have established a strong pro‐inflammatory response in the brain in the acute to subacute stage of TBI, then tissue damage is likely to be exacerbated.…”

Section: Inflammation In Tbimentioning

confidence: 99%

Potential of mesenchymal stem cells alone, or in combination, to treat traumatic brain injury

et al. 2020

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Traumatic brain injury (TBI) causes death and disability in the United States and around the world. The traumatic insult causes the mechanical injury of the brain and primary cellular death. While a comprehensive pathological mechanism of TBI is still lacking, the focus of the TBI research is concentrated on understanding the pathophysiology and developing suitable therapeutic approaches. Given the complexities in pathophysiology involving interconnected immunologic, inflammatory, and neurological cascades occurring after TBI, the therapies directed to a single mechanism fail in the clinical trials. This has led to the development of the paradigm of a combination therapeutic approach against TBI. While there are no drugs available for the treatment of TBI, stem cell therapy has shown promising results in preclinical studies. But, the success of the therapy depends on the survival of the stem cells, which are limited by several factors including route of administration, health of the administered cells, and inflammatory microenvironment of the injured brain. Reducing the inflammation prior to cell administration may provide a better outcome of cell therapy following TBI. This review is focused on different therapeutic approaches of TBI and the present status of the clinical trials.

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Neutrophils in traumatic brain injury (TBI): friend or foe?

Cited by 115 publications

References 279 publications

The Brain Entangled: The Contribution of Neutrophil Extracellular Traps to the Diseases of the Central Nervous System

The Brain Entangled: The Contribution of Neutrophil Extracellular Traps to the Diseases of the Central Nervous System

Peripheral Immune Response Following Traumatic Brain Injury

Potential of mesenchymal stem cells alone, or in combination, to treat traumatic brain injury

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